■•■}■■ ■■ ■:';'.f;;|vlh, IfJSSH? l ' v£IS I ; * '■J ??»?: :» '■'■■.lip N»t:0N1i IliDARV OF MFDiCINE NLII DD13bE3fi b NLM001362386 ■h Z' rs> 'r The SPECIAL PATHOLOGY and TREATMENT -OF- THE ORGANIC Diseases He Stomach, ■BY- JOHN C. HEMMETER, M.B., M.D., Phil. D. CLINICAL PROFESSOR of MEDICINE in^he BALTIMORE MEDICAL COLLECIi; LM^^^.M7z^f7y t^ CONSULTING PHYSICIAN to the MARYLAND GENERAL HOSPITAL. _ ' /Vt Q-c+yXo. -If S LI BRXRY * j IN TWO PARTS. ! SURGEON GENERALS OFFICE | FES. 5—1903 Published by P. Blakiston, Son & Co., Philadelphia, Pa. Press ok V. Ruzicka and Sons, Bookbinders and Printers, 501 N. Gay St. BALTIMORE, MD. 1897. "H4S9s 1897 / ^£r COPYRIGHTED 1897 ---BY--- P. BLAKISTON, SON & CO. PHILADELPHIA. ^m: TO MY GOOD FATHER, Mr. JOHN HEMMETER, AND MY FATHERLY FRIEND, MR. CHARLES HILGENBERG, THIS VOLUME IS GRATEFULLY DEDICATED. m PEEFAOE. ||l| N AN ADDRESS before the Medical and Chirurgical State /",j Faculty of Maryland in April 1896, Professor Da Costa in *w$ speaking of the manner in which Medical Libraries build up and increase, said that "Books attract books, and as a rule, any new work in any particular class has a striking family resemblance to those already published." If this new contribution to the Pathology and Treatment of Organic Diseases of the Stomach does not conform to Da Costa's generalization, it is not because of any premeditated plan to make it different from other works on the same subject, but because a number of entirely new methods of diagnosis have entered into it, and, because an effort has been made to do justice to the work of American Clinicians on this special department, which foreign books, as a rule omit, except in-a few instances where the American con- tribution is so indispensable that they can not consistently avoid reference to it. When the printing of this book was begun, there was no work of American origin on this subject. Since then the volume by Max Einhorn has appeared as the pioneer. This small volume is printed from the advance sheets of a lar- ger and more exhaustive work to be published in October,1897and has been compiled for the benefit of the author's class at the Balti- more Medical College. We already have a large number of eminently qualified and versatile clinicians, men with acute observing powers and analytical minds who have worked in this interesting field. The names of Austin Flint, Pepper, Osier and Delafield are as well known in this department in our country, as those of Kussmaul, Senator, Leube and Ewald in Germany. The work of Einhorn will mark an epoch in the history of gas- tro enterology in this country, ably supplemented and supported by the researches of D. D. Stewart, Charles G. Stockton, Allen Jones, Julius Friedenwald, Francis P. Kinnicut, Charles E. Simon and other gifted experimenters and observers. The Surgery of the Alimentary tract has many very creditable representatives in our country among whom may be mentioned, Robert F. Weir, N. Senn, McBurney, Roswell Park, F. Lang, R. Abbe, W. Meyer, Murphy, Bull, Maurice H. Richardson, Gerster, John M. T. Finney. The literary and practical contributions of a number of these men has reached a classic standard and compelled foreign ad- miration. The Physiological Chemistry of Digestion and Internal Secre- tion has received the benefit of the work of Bowditch, Chittenden, Howell, Vaughn, Adami, Able and others, and Dietetics has its ver- satile representative in Gilman Thompson. To Dr. Edward L. Whitney, my associate, it becomes my pleas- ant duty to express thanks for the manner in which he has written the chemical section of Part first and much kind assistance through- out the work. Pathology has its men now universally acknowledged for the integrity and dignity of their work in our esteemed teachers Welch and Councilman. Already an American School of Pathology is forming with these men, and Prudden, Flexner and others. But in the special Pathology of the Digestive organs, the workers are few, a very creditable beginning however, has been made; the foundation is an honor to the prospective builders, — The land to be explored is exceedingly large in its extent,— "The harvest is plenteous, but the laborers are few." ''Heard are the voices, Heard are the sages, The worlds and the ages; Chose well, your choice is Brief and yet endless." "Here eyes do regard you In eternity's stillness, Here is all fullness, Ye brave to reward you, Work and despair not." (Goethe ) FVART FIRST. ANATOMY AND PHYSIOLOGY OF THE DIGESTIVE ORGANS. The METHODS AND TECHNICS OF DIAGNOSIS. LECTURE I. THE ANATOMY OF THE STOMACH AND INTESTINES. («) THE STOMACH. THE STOMACH is the dilated, sac like portion of the digestive tract, between the oesophagus and small intestine; one can distinguish a lower convex arch, the greater curvature which is directed toward the left and downwards, and an upper concave arch, the lesser curvature, which is directed toward the right and upwards; the broad left end of the greater curvature is called the fundus, whose size varies according to age. Between this and the lesser curvature is situated the cardia, this is the boundary between the oesophagus and the stomach, and while it is not marked on the outside of the organ, there is a distinct limiting line internally on the mucous membrane, which is caused by a change in the struct- ure of the epithelial lining. It is now well known that at this point the arrangement of the muscular fibers and veins is also different from that in the oesophagus. The location of the cardia in the adult is at the twelth thoracic vertebra; at about the height of the birfucation of the bronchi; the spiral curving of the oesophagus around the aorta begins, by exe- cuting this curve, the convexity of which is towards the right, the oesophagus gets to the left side of the aorta, and passes through the diaphragm in the foramen oesophageum near the spinal column. The stomach becomes narrower from the fundus towards the pylorus; near the pylorus there is a constriction caused by a ring- like formation of muscular tissue, which corresponds to the pyloric valve; the muscular tissue is covered internally by the gastric muc- 2 — ous membrane, the latter forming the pyloric valve; the opening of this valve is of varying diameter; the part of the stomach preceed- ing the pylorus is called the antrum pyloricum, and is frequently separated from the greater curvature by an indentation or depres- sion, this antrum may be elongated so as to assume resemblance to the intestine which is frequently the case in the female sex. On the anterior and posterior wall of the stomach running along between the muscular and serous coat of the organ, are two band-like stripes, consisting of elastic, smooth, muscular fibers, these are the pyloric ligaments. The size of the stomach depends upon the age, sex, individual- ity and degree of its distention. In the female sex it is generally small and more slender; the long axis extends from twenty-five to thirty-five c. m. The greatest vertical measurement at the cardia is fifteen cm., and the greatest straight diameter is eleven to twelve; the smallest at the antrum pyloricum is from three to four centi meters. The capacity Varies considerably; Ewald considers that sixteen to seventeen hundred c. c. is the normal limit; $i of the stomach belong to the left body half, and % to the right. The cardia is located behind the median edge of the fifth and sixth ribs. The fundus, the largest part of the body, is in the left hypochondrium; the rest with the pyloric part is in the epigastrum. The pylorus lies in the right half of the body, but occasionally changes to the middle line at the level of the seventh and eighth ribs, in a line with the ensi-form cartilage. The lesser curvature runs along to the left and near to the spinal column. The vaulting dome of the fundus, which applies itself to the concavity of the diaphragm is the highest point; the deepest point of the stomach is in the greater curvature; in the inferior % of a straight line connecting the ensiform cartilage with the umbilicus; both the highest and lowest part of the stomach are moved about according to the level of the diaphragm and the disten- tion of the stomach; In an empty condition, the stomach is withdrawn into the upper portion of the abdomen, but when filled it extends in all directions, but mostly in the direction of its long axis, from the left above to right downwards, in a state of moderate distention, about forty c. m. of its anterior wall come in contact with the inner surface of the anterior abdominal wall. The diaphragm covers the fundus and the largest part of the 5 — left segment, while the left lobe of the liver up to the sulcus interlo- bularis covers over the smaller part, that is, the lesser curvature and the pyloric portion. From this fact arises the difficulty to palpate tumors in the latter place, which is impossible, except when in gastroptosis, descent of the stomach moves it away from the liver; in the state of expansion or dilatation the stomach moves out from behind the liver, but the lesser curvature cannot change its location to any considerable extent, and the change of location of the whole stomach caused by filling, is produced almost exclusively by an ex- tension of the greater curvature. The pancreas extends along the posterior wall of the stomach; at the upper edge of the pancreas are the lienalis artery and vein. The transvers colon runs along the greater curvature, and its left flexure fills the remaining space in the left hypochrondium. The location of the stomach is fixed by a ligamentous attachment of the cardia, and the pylorus, and also by a number of suspensory liga- ments, which are all formations of the peritoneum; some authors say that the stomach is supported in this position by intra-abdominal pressure; the experiments of Moritz of Munich, and myself have proven that intra-abdominal pressure adds nothing to the support of the stomach. The gastro-phrenic ligament which towards the right passes into the lesser omentum, and towards the left extends into the phrenico-lienal ligament surrounds and embraces the cardia; the cardia sits lower than the fundus, and its situation corresponds to the upper end of the sixth and seventh costal cartilages, or to the level of the ninth thoracic vertebra; this part of the stomach is there- fore moved to the left of the middle line, and next to the spinal column; at about the level of the twelfth thoracic and first lumbar vertebras, here it is fixed to the lumbar part of the diaphragm. The greater omentum arises from the large curvature. The posterior fold of this omentum forms the meso-colon transversum; ---- This is the reason why changes of location in the greater omentum (hernia and inflamma- tory adhesions) can produce traction of the stomach, as the stomach is really attached only at the cardia, and the pylorus adhears to the posterior abdominal wall, by the descending portion of the duo- denum; the stomach is capable of being moved about, not so much in its entirely as in its parts (the great curvature for instance). The stomach has a complete peritoneal covering, which consists of an an- -- 4 terior and posterior layer, these layers uniting at the two curvatures of the stomach to form the lesser and greater omentum; between these two layers a space is left for the blood and lymph vessels of the stomach. The muscular stratum contains three kinds of fibers longitudinal, transverse, and oblique. The longitudinal layer of muscular fibers, a continuation of those of the oesophagus, presents a denser arrange- ment at the lesser curvature than at the greater, and forms the lig- amenta pylorica at the pyloric part, which are bands of muscular fibers, expanded and broadened out, not ligaments in the real sense of the word. . The circular layer of muscular fibers is placed internally to the longitudinal layer, the fibers of which are crossed at right angles. The fibers of this circular layer are placed around the stomach in a ring, or belt like manner; at the pylorus it shows a local thickening of the muscle rings, the sphincter pylori; a fold of the mucosa to the innermost side of this sphincter constitutes the pyloric valve. The longitudinal fibers also have a part in the formation of the sphincter, for whilst the superficial layer of longitudinal fibers passes. on over the pyloric sphincter into the duo-denum, the deeper long- itudinal fibers enter the pyloric valve and encircle and grasp the cir- cular fibers in a loop like manner (Dilator Pylori —Rudinger). The cardia has no special sphincter, but the oblique fibers, cross and de- cussate at the periphery of this portion. As the sphincter pylori is contracted during digestion, gas and liquids can readily escape through the cardia. The oblique fibers are limited chiefly to the cardiac end of the stomach, where they are disposed as a thick uni- form layer, some passing oblivuely from left to right, others from right to left around the cardiac orifice. The submucosa, or cellular coat of the stomach consists of a loose filamentous, areolar tissue, and loosely binds the mucosa to the muscular layers. The most important, and interesting is the mucous layer, or mucous membrane proper of the stomach; it is a thick layer with a smooth soft velvety surface. During infancy, and immediately af- ter death it is of a pinkish tinge, but in adult life and old age, it becomes af a pale straw or ash grey color; at the pylorus it is much thicker than at the cardia. During the contracted state of the organ, it is thrown into numerous plaits or rugae, which, for the most part, — 5 has a longitudinal direction, and are most marked towards the lesser end of the stomach, and along the greater curvature; these folds are entirely obliterated when the organ becomes distended. STRUCTURE OF THE MUCOUS MEMBRANE. When examined with a lens, the inner surface of the mucous membrane presents a peculiar honey-comb appearance, from being covered with small shallow depressions or alveoli, of a polygonal or hexagonal form, which vary from one one-hundredth to one three- hundred and fiftieth of an inch in diameter, and are separated by slightly elevated ridges. In the bottom of the alveoli are seen the orifices of minute tubes, the gastric follicles, which are situated per- pendicularly side by side, in the entire substance of the mucous membrane; they are short and simple, tubular in character, toward the cardia; but at the pyloric end, they are longer, more thickly set convoluted, and terminate in dilated saccular extremities, or are subdivided into from two to six tubular branches. Watney has pointed out that these convoluted, or coiled tubes form the transition from the simple tubular follicles, to the convoluted glands of Brunner, which lie immediately below the pylorus. The gastric follicles are composed of a homogeneous base- ment membrane, lined upon its free surface by a layer of cells, which differ in their character in different parts of the stomach. Towards the pylorus these tubes are lined throughout by columnar epithelium; they are termed the mucous glands, and are supposed to secrete the gastric mucous. In other parts of the organ, the deep parts of each tube is filled with nuclei, and a mass of granules; above these are a mass of nucleated cells, the upper fourth of the tube be- ing lined by columnar epithelium: These are called the peptic glands, and are the supposed agents in the secretion of gastric juice. Simple follicles are found in greater or less number over the entire surface of the mucous membrane; they are most numerous near the pyloric end of the stomach, and are especially distinct in early life. The epithelium lining the mucous membrane of the stomach and its alveoli is of the columnar variety. VESSELS AND NERVES. The arteries supplying the stomach are, the coronaria ventriculi, the pyloric and right gastro-epiploic branches of the hepatic, the left — 6 — gastro-epiploic and vasa brevia from the splenic. They supply the muscular coat, ramify in the submucous coat, and are finally distri- buted to the mucous membrane. The arrangement of the vessels in the mucous membrane is some-what peculiar. The arteries break up at the base of the gastric tubules into a plexus of fine capillaries which run upwards, between the tubules, anastomosing with each other, and ending in a plexus of large capillaries, which surround the mouth of the tubes, and also form hexagonal meshes around the alveoli; From these latter the veins arise, which pursue a straight course back to the submucous tissue, between the tubules, to termi- nate in the splenic and portal veins. The lymphatics are abundant and may be classed into a super- ficia and deep set, which pass through the lymphatic glands found along the two curvatures. The nerves are supplied from the- right and left pneumogastric, and numerous branches from the abdomi- nal sympathetics. Usually 4 to 6 gland openings are found at the base of each follicle. According to Sappey there are 5,000,000 of these glands in the organ, for which reason the gastric mucosa may justly be considered a continuous gland that is spread out into a flat surface. —(Hyrtl and Luschka). The gland tubules are as long as the en- tire thickness of the mucosa, and their sac-like and branched bases extend into the muscularis mucosa, the action af these muscular fi- bers assist in the evacuation of the tubules during digestion; These ends of the tubules extending into the muscular layer are usually branched. The cylindrical epithelium of the surface of the stomach which is separated from the pavement epithelial lining of the oesophagus by a distinct but irregular line at the beginning of the cardia, — is found also in the beginning of the tubules, but only extends down- ward to Y\ or Yi their length; from this point downward they are no longer observed, but two different kinds of cells are now seen to line the glandular tubule. One of the variety of lining cells of the gland tubules is located toward the axis of the tube, and is known as the adelomorphous cells of Rollet, because they show no cell contours or outline in the fresh state, called by Haidenhayn chief cells, they have a cubical, cylindrical form and indistinct nuclei; the second variety shows larger round cells, delomorphous cells of Rollet, — 7 — also parietal cells, which in the fresh state show a finely granular contour, which becomes sharply outlined on addition of water or salt solution, they show coarsely grained contents and a distinct nucleus. The first form, the cubical or cylindrical chief or adelo- morphous cells, are supposed to secrete the ferments pepsin and rennet; the second form, the larger round delomorphous cells or parietal cells, are supposed to secrete the HCL. LECTURE II. HISTOLOGY OF THE STOMACH AND INTESTINES. SHE PEPTIC GLANDS consist of a duct, a neck and a fundus; the latter is the deepest portion, and is often divided. These tubular glands have a distinct membrana propria separating them from the loose areolar connective tissue of the submucosa, in which they lie. THREE KINDS OF CELLS OF THE PEPTIC GLANDS. First, cylindrical cells of the gland duct and pit; lining Y\ to Yi of the distance from the surface of the mucous membrane down- ward. A continuation of the cylindrical epithelium of the general internal surface of the gastric mucous membrane, these cells seem to secrete mucous only. Second, lightly colored, pyramidal or cu- boidal cells with a granular protoplasm and sperical nucleus. These cells do not stain with aniline, and were termed adelomorphous cells by Rollet, — because they show no cell contours in the fresh state. Rosenheim states that they are almost clear and transparant during fasting, and become cloudy and granular during digestion. Haiden- hayn designated them as the chief or central cells, and they were held by him to be the formers of the ferments, pepsinogen, and Rennet — Zymogen. These chief or central cells touch the lumen of the duct more extensively than the next following variety, the— —Third, kind of peptic cells is known as the border, or partial cell, because they rest upon the membrana propria with much broader — 8 — bases than the chief or central cells, for this very reason they par- ticipate to a less degree in the limitation of the lumen of the duct; they are generally round or triangular, finely granular, and stain intensely with aniline, and were designated by Rollet as delomor- phous cells; Haidenhayn supposes them to be the formers of hydro- chloric acid. If we assume for the sake of locating these various cells; a division of the tubule into four sections, beginning at the portion nearest the submucosa, we shall have the {«) fundus of the gland tubule, then the (&) outer secretory portion, the (<■) inner secretory portion and opening on the inner surface of the mucosa, the (d) alveolus;—Then one finds the border, parietal, delomorphous or aniline cells in the outer secreting portion most numerous, and becoming scarce in the fundus or end portion. Haidenhayn asserted that there were no border cells in the fun- dus at all, but this has been denied by Stohr, Kupffer and Boas. The number of border or acid cells depends upon the stage of di- gestion, as this function proceeds the border cells increase, and the chief, central, or ferment cells diminish in number, it would thus seem as if the border or acid cells, formed out of chief or ferment cells with the advance of digestion. In a fasting state the chief cells are largely in excess. Haidehayn's conclusions, that the chief or central cells are producers of the digestive ferments, and the border or aniline staining cells produce the hydrochloric acid, have bee con- firmed by a number of other observers (Grutzner, v Swiezicki, and recently Sehrwald). Their method of experimentation was mainly the following; It is known that the glandular tubules of the pyloric region contain only chief or central cells, producing ferments only, and no acid, whilst the gland tubules of the fundus contain both central cells, and also border or acid cells. Now Haidenhayn succeeded in a number of dogs to dissect, and remove the pyloric portion of the stomach en- tirely, and to heal the organ into an external abdominal wound. In other dogs he removed the fundus entirely, leaving the pyloric por- tion intact, and succeeded in making this altered stomach without a fundus heal the external abdominal wound. He therefore had two kinds of operated animals with stomachs opening on the abdomen. After this it was found that animals in which the pyloric region was excised furnished a juice that contained — 9 — both acid and pepsin, these were therefore produced by the glands of the fundus which contain both varieties of secretory cells. In the animals, however, that had been deprived of the fundus by ex- cision, and the only secretory surface that was left being the pylor- ic region, it was found that an alkaline juice was secreted contain- ing only ferments; that this juice did contain pepsin was proven by its power of digesting fibrin when hydrochloric acid was added to it. Now as the gland tubules of the pylorus contain only chief or central cells, that do not stain with aniline, the couclusion is justifi- able, that, these chief cells secrete only ferments and that therefore the border or aniline staining cells must secrete the hydrochloric acid. It has been found that the border or acid cells, called also the oxyntic cells,— are in communication with the central canal of the gland tubule by a tiny little canaliculus, an extension from the cen- tral lumen of the gland, to, or into the oxyntic or acid cells. These canaliculi were brought out by Golgi with his silver stain. THE SMALL INTESTINE. The small intestine commences at the pylorus, and, after many convolutions, terminates in the large intestine. It measures on an average, about 22 feet in length in an adult, and becomes gradually narrower from its upper to its lower end. Its convolutions occupy the middle and lower parts of the abdomen, and also frequently de- scend into the pelvis. The small intestine is devided into three portions, which have received different names. The first ten to twelve inches immediate- ly succeeding the stomach, and comprising the widest and most fixed part of the tube, is called the duodenum. This part is further distinguished by its close relation to the head of the pancreas,and by the absence of a mesentery. The remainder, which is arbitrarily divided into an upper two-fifths called the jejunum, and a lower three-fifths called the ileum, is very convoluted and movable, being- connected with the posterior abdominal wall by a long and exten- sive fold of peritoneum called the mesentery, and by numerous blood vessels and nerves. Although there is no distinct line of demarca- tion between the jejunum and the ileum, yet the portion of the small intestine included under these two names gradually undergoes cer- tain changes in structure and appearance from above downwards, — 10 — so that the upper end of the jejunum can readily be distinguished from the lower part of the ileum. STRUCTURE OF THE SMALL INTESTINE. The small intestine, like the stomach, is composed of four coats, viz., the serous or peritoneal, muscular, areolar, and mucous. The external or serous coat almost entirely surrounds the intes- tinal tube in the whole extent of jejunum and ileum leaving only a narrow interval behind, where it passes off and becomes continous with the two layers of the mesentery. The line at which this takes place is named the attached or mesenteric border of the intestine. The duodenum, on the other hand, is but partially covered by the peritoneum. The muscular coat censists of two layers of fibers; an outer longitudinal, and an inner or circular set. The longitudinal fibers constitute an entire but comparatively thin layer, and are most obvious along the free border of the intestine. The circular layer is thicker and more distinct. The muscular tunic becomes gradually thinner towards the lower part of the. small intestine. It is pale in color, and is composed of plain muscular tissue, the cells of which are of considerable length. The progressive contraction of these fibers, commencing at any part of the intestine, and advancing in a downward direction, pro- duces the peculiar vermicular or peristaltic movement by which the contents are forced onwards through the canal. In the narrowing of the tube the circular fibers are mainly concerned, the longitudinal fibres tending to produce dilatation (Exner); and those found along the free border of the intestine may have the effect of straightening or unfolding its successive convolutions. There is a gangliated plex- us of nerve-fibres and a network of lymphatic vessels between the two muscular layers. The submucous coat of the small intestine is a layer of areolar tissue of a loose texture, which is connected more firmly with the mucous than with the muscular coat. Within it the blood-vessels ramify before passing to the mucous membrane, and there is a gan- gliated plexus of nerve-fibers and a network of large lymphatic vessels in it. The internal coat or mucous membrane is characterised by the finely flocculent or shaggy apearance of its inner surface resembling — li- the pile upon velvet. This appearance is due to the surface being thickly covered with minute processes named villi. It is one of the most vascular membranes in the body, and is naturally of a reddish color in the upper part of the small intestine, but is paler, and at the same time thinner, towards the lower end. It is lined with col- umnar epithelium throughout its whole extent, and next to the submucous coat is bounded by a layer of plain muscular tissue (muscularis mucosa); between this and the epithelium the substance of the membrane, apart from the tubular glands which will be after- wards described, consists mainly of retiform tissue which supports the blood-vessel, nerves, lymphatics and lacteals, and encloses in its meshes numerous lymph-corpuscles. VALVULE CONNIVENTES. The mucous membrane, in addition to small effaceable folds or rugae, possesses also permanent folds, which cannot be obliterated, even when the tube is forcibly distended. These permanent folds are the valvule conniventes or valves of Kerkring. They are cre- scentic projections of the mucous membrane, placed transversely to the axis of the bowel and following one another closely. The ma- jority of the folds do not extend more than one-half or two-thirds around the interior of the tube, but it has been shown by Brooks and Kazzander that some form complete circles, and others spirals, The spiral forms may occur singly or in groups of two or three. They generally extend a little more than once around the bowel, but in rare cases may go round two or three times. At their highest point they project inwards for about a third of an inch. Some of the valvule conniventes are bifurcated at one or both ends, and others termi- nate abruptly. Each consists of a fold of mucous membrane, that is, of two layers placed back to back, and united together by sub- mucous areolar tissue. They contain no part of the circular or lon- gitudinal muscular coats. Being extensions of the mucous membrane they serve to increase the absorbent surface to which the food is exposed. The valvule conniventes are not uniformly distributed over the various parts of the small intestine. There are none quite at the commencment of the duodenum; a short distance from the pylorus they begin to appear; beyond the point at which the bile and pan- — 12 — creatic juice are poured intothe duodenum they are very large, reg- ularly crescentic in form, and placed so near to each other that the intervals between them are not greater than the breadth of the valves; they continue thus through the rest of the duodenum and along the upper half of the jejunum; below that point they begin to get smaller and farther apart, and finally, towards the middle or lower end of the ileum, having gradually become more irregular and indistinct, sometimes even acquiring a very oblique direction, they altogether disappear. The villi, peculiar to the small intestine, and giving to its inter- nal surf ace the velvety appearance already spoken of, are small pro- cesses of the mucous membrane, which are closely set on every part of the inner surface over the valvulae conniventes, as well as between them. Their length varies from 0.5 mm. to 0.7 mm. or sometimes more. They are largest and most numerous in the duodenum and jeju- num, and becomes gradually smaller, and fewer in number in the ileum. According to Rauber, they are short and leaf-shaped in the duodenum, and as the gut is followed downwards they become gradually longer and thinner, so that they are tongue-shaped in the jejunum, and filiform in the ileum. Occasionally two or three are connected together at their bases. In the upper part of the small intestine there are from 10 to 18 villi in a square millimeter, and in the illeum from 8 to 14 in the same space. This would give about four millions altogether (Krause.) A villus consists of a prolongation of the proper mucous mem- brane. It is covered by columnar epithelium, and encloses a network of blood-vessels, one or more lymphatic vessels (lacteals), and a few longitudinal plain muscular fiber-cells, these being all supported and held together by retiform lymphoid tissue. Under the epithelium is a basement membrane composed of flattened cells, which on the one hand are connected with the branched cells of the retiform tissue and on the other hand send processes between the epithelial cells. Nervous fibrils penetrate into the villi from the plexus of Meissner and form arborizations through- out their whole substance. Each villus receives as a rule one small arterial twig, which runs from the submucous coat, through the muscularis mucosae to the - n - base of the villus and then up the centre to near the middle line of the villus where it begins to break up into a number of capillaries. These form near the surface, beneath the epithelium and limit- ing membrane, a fine capillary network, from which the blood is returned for the most part by one or two venules, which in man commence near the tip of the villus and pass down to its base to join the venous plexus of the mucous membrane, whence the blood is conveyed to the large veins of the submucosa. The lacteal lies in the centre of the villus and in the smaller villi is usually a single vessel with a closed and somewhat expanded extremity and of considerably larger diameter than the capillaries of the blood vessels around. In the human subject there are never more than two intercommunicating lacteals in a single villus. The lacteals in the villi are bounded by a delicate layer of flat- tened epithelial cells; these are connected with the branched cells of the tissue of the villus, and these again with the flattened cells form- ing the basement membrane; from the latter, prolongations extend between the epithelium cells toward the surface. Briicke first dis- covered the muscular tissue within the villus, consisting of unstriat- ed plain fibre cells, disposed longitudinally around the lacteal. In animals a very evident retraction of the villus is noticeable when these muscular fibers which are prolongations from the muscularis musosae are stimulated. The fiber cells at the sides and towards the end of the villus pass from the lacteal to be attached to the basement membrane in a bifurcating manner. Columnar epithelial cells cover not only the villi but also the rest of the surface of the small intestine and extend into the tubular glands. There is never any continuity between the extremity that is attached to the basement membrane and the branched corpuscles of the retiform tissue of the villus. This epithelium separates easily from the subjacent tissue. Between the cells composing it are a variable number of leuccocytes most numerous in the lower part of the intestines near the lymphoid follicles. Occasionally they are seen to be free in small lymph spaces between the columnar epithelial cells and showing indications of Karyokinesis. Hardy declares that immediately below the columnar epithelium of the villi, there is frequently a well marked layer of cells that take up the eosin stain — 14 — readily. Hence, he calls them eosinophilic. LECTURE III. HISTOLOGY OF INTESTINAL MUCOSA. MONG the ordinary epithelial cells of the villus are others, the outer half of which is filled with mucigen, and at times such beaker or cup shaped empty cells are observed from which this has been discharged as mucous, and the free end is ruptured; these are sometimes called the goblet cells. The number of cells containing mucous varies much in different animals and under diff- erent conditions in the same animal. There are comparatively few mucous eel's in the glands of the small intestine. The epithelial cells are as far as can be ascertained the principal agents in promoting the absorption of food materials from the inter- ior of the gut, and the seat of the retrograde processes of metabolism which the products of digestion undergo during absorption. Peptone when injected into the blood of an animal whose gastric juice has formed, it acts as a poison. It is due to these epithelial cells of the intestine that peptone is so modified by them during absorption that it becomes of use to the organism. Most food particles can not be traced in microscopic specimens, but fatty or oily substances, from their property of becoming stained with osmic acid can be to some extent followed out. The examin- ation of such specimens taken during digestion of a meal containing fat, shows the epithelial cells turbid with oil droplets in their inter- ior, and in some animals at a subsequent stage, amoeboid cells appear within the tissue of the villus pervaded with similar but finer fatty particles and eventually the central lacteal becomes filled with these. It is probable that these amoeboid lymph corpuscles appearing so abundantly within the villus and among the epithelial cells on its surface, play an important part in the transference of such particles from the epithelial cells in the lacteal, for at certain stages /» — 15 — of fat absorption, they contain abundant fatty particles. The large amount of lymphoid tissue in the lower part of the small intestine seems to be related to a greater power of absorption in that part. In the transference of carbon particles in the lungs, from the interior of the alveoli into the lymphatics, which at least in part is due to the action of amoeboid cells, we have an analogous process. GLANDS. Two kinds of true secreting glands are found in the intestine these are; (1) Glands or crypts of Lieberkiihn and the (2) glands of Brunner. In addition to these, there are found also two varieties of intestinal lymph follicles the (1) Solitary and (2) the Agminate glands, the latter often designated as Peyer's patches. Although the solitary and agminated lymph follicles have no ducts opening upon the inner intestinal surfaces, like Brunner's and Lieberkiihn's glands, they are nevertheless spoken of as glands. The follicles crypts or glands of Lieberkiihn are tubular pits lined by columnar epithelium, occuring between the villi and on the valvule conniventes. Here and there in these crypts, goblet cells occur in the epithelium. They are present throughout the large and small intestine, and extend through the entire depth of the mu- cosae, their ends approaching the muscularis mucosae. The duodenum possesses an additional layer of true secreting structures in the glands of Brunner. They would appear to repre- sent the direct continuations and higher specializations of the pyloric glands. In passing from the stomach into the intestines, these tub- ules undergo repeated division, at the same time sinking deeper into the mucosa, finally reaching below this layer to take up a position within the submucosa of the duodenum, underneath the overlying layer of the crypts of Lieberkiihn which are contained in the mu- cosa proper. Brunner's glands belong to the racemose type and under the microscope they consist of a number of tubular alveoli connected by terminal ramifications of the duct which penetrates the muscularis mucosae, and opens either between the mouths of the Lieberkiihn crypts or sometimes into their bases. The solitary glands are isolated lymph follicles scattered through the entire intestine, most abundant in lower ileum. Situated in the mucosa, at times in the submucosa; the lymphoid tissue in them is — 16 — denser toward the periphery, but is everywhere so closely packed that the supporting reticulum of connective tissue is masked. The agminated glands, or Peyer's patches are large oval groups of closely aggregated groups of lymph follicles held together by dif- fuse adenoid tissue, limited to lower Yz of the small intestine. De- velopment of these is most perfect in the ileum, appearing first v/ithin the mucosa, they later encroach upon the submucous tissue. Where the summits of these follicles impinge against the inner layer of the mucosa, the position of the agminated glands are indi- cated by an elevation corresponding to them on the mucous surface. In that case the villi are frequently pushed aside.. THE BLOOD-VESSELS OF THE INTESTINES. The vessels follow the general arrangement of those in the stomach; the larger ones piercing the serous and muscular coat, giv- ing off slender twigs to supply these tunics, and when they enter the submucosa, the vessels form a wide, meshed, network. Many branches then pass through the muscularis mucosae to be distributed to the deeper, as well as the superficial part of the mucosa. Around the tubular glands a network is formed by narrow capillaries, and just beneath the epithelium the capillaries become wider and encircle the mouths of the follicles. From this superficial capillary network the veins arise, and passing down between the follicles, join the deeper venous plexus, this in turn communicating with the larger veins of the submucosa. The villi have special additional arteries running to their bases, expanding into capillaries thar extend beneath the epithelium and around the central lacteal as far as the ends of the villi. These capillaries terminate in venous stems which descend almost perpen- dicularly into the mucosa in their course receiving the superficial capillaries encircling the gland ducts. Brunner's glands, and the solitary and agminated follicles are supplied from the submucosa by vessels terminating in capillary networks distributed to the acini of the glands and interior of the lymph follicles. The blood-vessels of the intestines taken as a whole, constitute a mighty vascular territory which is capable of taking up yi of the total amount of blood of the body. The arteries are all branches of the superior and inferior mesen- — 17 — teric arteries which run along and approach the gut in the mesen- tery. The intestinal veins form the principal portion of the portal artery system. LYMPH-VESSELS. The begining of the lymph-vessels can be traced to the lacteals within the villi, where they begin as tiny little blind pouches at the apex of the villus. In some broad villi there are two or three such lymph-vessels that anastomose with one another. From here they run down in the septa between the glands in the lymph-vessel mesh- work over the muscularis mucosae. This again anastomoses with an outer lymph-vessel network in the submucosae. Here already, the lymphatics begin to be provided with valves. The nerves of the intestine, like those of the stomach originate chiefly from the mesenteric plexus which is formed by branches from the coeliac plexus, the semilunar ganglion and vagus nerve. These nerve branches consist of medullated and nonmedullated fibers, that begin to form an abundant network under the peritoneum of the intestine, then penetrate the longitudinal muscular stratum and between this and the circular layer form a peculiar plexus with nu- merous microscopic ganglia; they are called the plexus of Auerbach. In the submucosa a similar network of fibers and ganglia has been termed Meissner's plexus. From Meissner's plexus very fine fibers are spun about the Lieberkiihn crypts, villus and limiting membrane. RELATIONS OF THE DUODENUM. This part of the gut in the adult is horse-shoe shaped, general- ly presenting well marked angles which divide it into four parts having four distinct directions, these are the (1) horizontal or su- perior part running backwards from the pylorus, to the right, in contact with the quadrate lobe of the liver, to the underside of the neck of the gall bladder where it curves sharply downwards to join the second part. This first or horizontal part is about 2 inches long when the stomach is empty. (2) The second or descending portion is about three inches long and commences just below the neck of the gall bladder opposite the right side of the first lumbar vertebra and passes down to the level of the third or fourth lumbar vertebra - 18 — where it turns sharply inwards to join the third part. (3) The third or transverse portion is between two to three in. long; beginning at the right of the third or fourth lumbar vertebra, it crosses over to the left side with a slight upward inclination and ends to the left of the aorta by curving upwards to join the terminal (4) fourth or ascend- ing portion which is about two inches long; it passes upward to the left side of the aorta as high as the upper border of the second lum- bar vertebra; here it turns abruptly forwards to join the jejunum, forming the duodenojejunal flexure. Thus the end of the duodenum is brought to the same level as the beginning. It has been compared to a trap its ends being always higher than its middle, which is thus fitted to retain the fluid poured into it from the liver, pancreas and its own glands, besides that which it receives from the stomach. — 19 — JEJUNUM AND ILEUM. The upper two-fifths of the remaining intestine immediately following the duodenum are called the jejunum, the lower three- fifths of the remainder, the ileum. Both are attached to the poster- ior abdominal wall by an extensive fold of peritoneum and the mesentery. The jejunum lies above and to the left of the ileum, but the coils are so irregular, that the position of any individual loop affords but little clue to the part of the intestine to which it belongs. The large intestine consists of the coecum, the colon and the rectum. The colon is subdivided according to the directions it takes into four parts which are the (1) ascending, (2) transverse, (3) de- scending and (4) sigmoid colon or flexure. The end of the ileum which rises out of the pelvis to the right ileac fossa, is not inserted into the beginning of the large intestine, but above the beginning and at the side of it. The part of the large intestine below this insertion is a blind pouch, the coecum. From the inner and back part of the coecum a little below the ileo colic opening, a narrow, round, worm like process about two or three inches, long is given off, the vermiform appendix. The coecum continues upward into the ascending colon which rises up in front of the right kidney to the edge of the liver, then this same large intestine passes beneath the greater curvature of the stomach, horizontally across to the left side as the transverse colon, here at the lower border of the spleen it turns downward as the descending colon. This large gut describes two right angled curves, the right and left colonic flexures fixed by the hepato colic and gastro colic ligaments respectively. The descending colon continues into the sigmoid colon or flexure which connects it with the rectum. The rectum following the curves of the sacro iliac symphysis and of the hollow of the sacrum itself has two curves;—an upper larger curve, concave anteriorly and a lower smaller curve, convex anteriorly. Only coecum, transverse colon and sigmoid have a complete peritoneal covering, the rest of the large gut is only covered anter- iorly. From the third sacral vertebra on, the rectum has no perito- neum. Those parts having no complete peritoneum, therefore have — 20 — no mesentery and are not very movable. The longitudinal fibers are contracted or narrowed down to 3 parallel bands. (Fasciae Tae- niae or lig. coli.) One of these bands runs along the attachment of the gastro colic ligament on the transverse colon, [fascia omentalis] the second along the mesenteric border and the third is free. Running down into the rectum these bands become so broad that they occupy the entire periphery of the tube. These longitudi- nal bands are much shorter than the other layers of the intestinal wall, which arrangement results in the characteristic sacculation of the large intestine. In the lower part of the rectum the circular muscular layer becomes thickened to form the internal anal sphincter of involuntary fibers. The external sphincter is composed of striated voluntary mus- cle fibers. The histology of the large, differs from that of the small intestine by the absence of the villi and larger size of the crypts and follicles. Several longitudinal elevations over the anus are called the columns of Morgagni; from this point downward the cylindrical epi- thelium ceases and flat pavement epithelium takes its place. LECTURE IV. PHYSIOLOGY OF DIGESTION. THE SIMPLE chemical elements of the various food substances namely C. H. N. S. and P. are not assimilable as such, because the human body is not capable of constructing higher com- pounds from them synthetically. It is compelled to take in these compounds in form of proteid or albuminous substances, carbohy- drates or starches and fats together with such inorganic bodies as water and salts. Even these foodstuffs which are essential for the maintenance and developement of the organism are not ingested as such but are contained together with innutritious materials in the various articles of diet which we derive from the animal and vegetable kingdom. — 21 — The innutritious admixtures of the food substances are not harmful, but are important as stimulants to the intestinal mucosa and to evacuation of feces. Amoung these innutritious substances are classed the connective tissue, the cartilages and tendous of meat and the cellulose of plants. Water plays a most important role in the economy of the body, for it goes to make up 60 per cent of the total organism. We loose about 2Y2 litres of water in 24 hours, through insensible perspira- tion, secretion and by defecation. About 300-400 grammes of water are formed by oxidation of food substances in 24 hours; so we have a deficit of 1500-1600 grammes, which must be supplied by the daily consumption of a corresponding amount of water; this occurs principally by the use of drinking water after we have taken in part of it by our foods or in shape of beverages. (Soups, milk, fruits, vegetables, potatoes, beer, wine, coffee, tea, etc.) Of mineral substances we must supply the daily loss of sodium chloride and other salts, particularly compounds of iron; these are normally introduced in sufficient quantities in food and drink. The chief constituents of food, Albuminous bodies, fats and carbohydrates, are of organic nature. The proteids or albuminous bodies and the fats are derived partly from the animal and partly from the vegetable kingdom. The carbohydrates are almost exclu- sively derived from the vegetable kingdom. The former serve the building up of the organism, and the continuance of life processes. The latter are producers of heat by their oxidation, which finally reaches HCO3 and H2O and are the prevailing sources of work. In addition to these a number of other substances occur in the food that are oxydized and might serve as sources of energy, these are the nitrogen free vegetable acids, the amido acids and alcohol for instance; quantitatively however they are not important. Other organic bodies that are contained in food materials as normal constituents, are Kreatin in meat, Glucosides, Alcaloids and ethereal oils in vegetables and spices, pass through the body with- out being oxydized or assimilated; they are not food substances, as they do not enter the metabolism of the body nor do they de- velope energy by chemical transformation. However a number of these are of importance in nutrition as they render the food more palatable and stimulate the secretions and the motility of the diges- — 22 — tive tract. In another place I said that the elements S.P.Cl.K.Na.Ca.Fe.Mg., are not food materials, but it must not be understood that they are entirely useless. They have some significance in the construction of tissue, although the organism can derive no energy from them, as they are always taken, in a highly oxydized state and leave in the same condition. Nevertheless the body will come to grief, if any one of these elements is excluded from the food. A certain mininum of these elements—the amount has not yet been ascertained—is absolutely necessary. Outside of the substances named above the food contains a number of materials, that are not at all absorbable or digestable and leave the digestive tract in an unchanged form; this is the slag and dross of the food and is taken into the body with vegetables. The normal, adult human organism daily looses by its metabolism, 120 grms. of Albuminous or proteid bodies, 80 g. fat, 400 g. carbohydrates, 25 g. salts and 2>2 litres of water. According- ly a corresponding amount of foodstuffs must be introduced in the diet. The articles of food contain these nutritious substances in a variety of proportions. The rational combination of these substan- ces is one of the objects of dietetics. Gilman Thompson in his new book on Dietetics, devides foods into six groups as follows; I. Wat- er, n. Salts, m. Proteids chiefly albuminous and allied gelatine, iv. Starches, v. Sugar, vi. Fats and oils. It still remains extremely difficult in the case of all foods, to trace their final uses in the body and determine with any accuracy, what proportions of each furnish respectively, energy, repair of tis- sue and heat, for there are no more complex chemical processes known than those of metabolism. [Gilman Thompson] Foods have three kinds of values: (1) Nutrient, (2) heat producing, (3).force producing values. The calculation of these different values, for each kind of food has been much simplified by the introduction of the conception of calories into the doctrines of nutrition. Formerly observers and investigators said, "A healthy man needs so many grms. proteid, so many grms. carbohydrates, so many grms. fat, etc. It was incon- venient to reckon with three magnitudes and to bring them into correct relation with the requisites of the individual organism. - 23 - Nowadays we compute the values of foodstuffs according to the physiological (kinetic) energy liberated in their oxidation. Ger- mans call this degree of energy which is always expressed in terms of heat the "Brennwerth," that means the value of food when it is burned in the process of metabolism, for this is nothing but a slow combustion. Now the unit for measurment of this heat energy of food is called a calorie. This capacity for heat production of foods is determined from the amount of heat which is liberated when any particular food substance is transformed from its original composi- tion when it entered the body,—by oxidation,—into those chemical combinations in which it leaves the organism. The unit for meas- urment is the calorie which signifies the amount of heat which is necessary to raise 1 kilogram of water, 1° centigrade. Now 1 gram of Albumen furnishes — 4.1 Calories. 1 " Carbohydrate " 4.1 " 1 " Fat " 9-3 1 " Alcohol " 7. Instead of saying a man requires 100 grms. Albumen, 100 grms. Fat and 400 grms. Carbohydrate, one now expresses this in calories thus;—A man requires 100 gr. Albumen x 4.1 ------ 410 Calories. 100 gr. Fats x 9-3------ 930 400 gr. Carbohydrate x 4.1 ------1640 Total 2980 For every kilogram of body weight an adult requires, when at rest,------ a food supply of 30—34 Calories. During light occupation " " " 34—40 » medium " " " " 40-45 " hard work " " " 45-60 In very adipose and obese person the requirements for food is less than the quantities stated by Y to #. If the above calculations of requisite number of calories per kilogram weight of any person is correct, and the supply maintained accordingly, the individual will maintain his weight. If the supply of calories is greater, he will gain weight, if the supply is less he will loose weight. In a condensed statement of facts like the present, it will be expedient to pass over the physiology of hunger, appetite and thirst, — 24 — and proceed at once to digestive actions. Digestion really begins in the mouth, where the food is chewed into small bits and is mixed with saliva, which mechanically facili- tates mastication and deglutition. Chemical transformation also begins here, for the diastasic ferment of saliva the Ptyalin trans- forms a small .portion of the starchy foods into sugar and maltose. Ptyalin can produce this transformation of starchy foods only in an alkaline medium, accordingly the action ceases in the stomach but not immediately however, as the conversion of starches into sugar goes on until the degree of acidity reaches 1 to the thousand, (1 pro mille.) As the ptyalin ferment becomes inactive in this acid- ity, the question arises, whether its activity is permanently destroy- ed by 1 pro mille acid or only temporarilly and whether it can re- sume its inverting power when the acid is neutralized. Boas who attempted a solution of this, came to the conclusion that subsequent alkalinization or diminution of the acid, causes the ptyalin to act again, so that in later stages of stomach digestion when the acid pro- duction ceases, the conversion of starch into grape sugar may be resumed. The existence of appetite is largely dependant upon the intact - ness of the salivary glands. In order to understand the various stages of starch conversion, it is essential for you to study the diges- tion of starch by ptyalin in the clinical laboratory. There are rec- ognized four stages of starch conversion, each distinct from the oth- er until dextrose is reached. 1. (a) These are common starch representing agluelikemucil- ageneous jelly, not a clear solution giving a dark blue color with iodine and iodide of potassium solution. The next stage shows the first action of ptyalin. 1. {b) Amidulin or Amylodextrin: This still gives a distinct- ly blue color though not so deep as No. \a with Lugols solution— but Amylodextrin is a soluble starch and represents a real solution. 2. (a) Erythro Dextrin:—Gradually as the inversion pro- gresses the color produced by the iodine solution becomes violet blue, violet, red violet, red or mahogony brown; this modification is called erythro dextrin, (b) Achroodextrin:—With continued ac- tion of the ptyalin, a substance is reached which gives no color with iodine; this is called achroodextrin. Amidulin is precipitated by [supplement] 24" Tables of Dietetics. Approximate Analyses of a Man (Moss). (Height, 5 feet 8 inches; weight 148 pounds. Oxygen — — — — 92.4 pou nds. Hydrogen — — — — 14.6 ' Carbon — — — 31.6 ' Nitrogen . _ — — 4.6 ' Phosphorus — — ■— 1.4 ' Calcium — — — 2.8 ' Sulphur — — — 0.24 ' Chlorine — — — 0.12 ' Sodium — — — 0.12 ' Iron — — — 0.02 ' Potassium — O.34 ' Magnesium — — — 0.04 ' Silica — — — — ? Fluorine — — — 0.02 • Total 148.00 pounds. Landois and Sterling give the following table, which differs some- what from the other tables in the relative proportion of fats and starches. An adult doing a moderate amount of work takes in as food per diem— c. H. N. 0. 120 grammes albumin, containing 90 grammes fats, containing 330 grammes starches, containing 64.18 70.20 146 82 8.60 10.26 20.33 18.88 | 28.34 ; 9.54 ___ 1 162.85 281.20 30.10 18.88 : 200 73 25' [SUPPLEMENT] Add 744.11 grammes 0. from the air by respiration " 2,818.00 " H20. 32.00 u inorganic conpounds [salts]. The whole is equal to three kilogrammes and a half [seven pounds], i. e., about a twentieth of the body weight, so that about six percent of the water, about six percent of the fat, about one percent of the albu- min, and about 0.4 percent of the salts of the body are daily transformed within the orgarnisms. An adult doing a moderate amount of work gives off in grammes: By respiration . By perspiration By urine............. By faeces........... Water. 330 660 1,700 128 2,818 c. „. N. o. 48.8 'J 651.15 2.6 7.2 9.8 3.3 15.8 11.1 20.0 3 0 3.0 12.0 281 6.3 681.45 standards f ,r Daily JJirfurirs, (Compiled by Atwater.) Weights of nutrients and calories of energy [heat units] in nutrients required in food per day. Nutrients. ! Children to a year and a half Children of two to six years— Children of six to fifteen years Aged women................................ Aged man...................................... Women at moderate work Voit Man at moderate work, Voit Man at hard work, Voit............ Man at moderate exercise, P^ ay fair Active labor, Play/air.............. Hard labor, Playfair................ Women with light exercise, Atwater Man with light ex1rc. Atwater Man at moderate work, '' Man at hard work, " Man at moderate " Moleschotl Man at moderate work, Wo/ff. Protein. Fats. Carbohy-drates. Total. energy. Grms. Grms. Grms. Grms Calories. 28 37 75 140 767 (20-36) (30-45) (60-90) 5.) 40 40 295 1,418 (36-70) (35-48) (100-250) 75 43 325 443 2,041; (70-80) (37-50) (250-400) . F 80 50 260 390 1,859 , 100 68 350 518 2.477 92 44 400 536 2.426 118 m 500 674 3,055 145 100 450 695 3,370 119 51 531 701 3,139 156 71 568 795 3.629 185 71 568 824 3,748 80 80 300 460 2,300 100 100 360 460 2,820 125 125 450 700 3,520 150 150 500 800 4,060 ] 30 40 550 720 3,160 120 35 540 605 3.032 [SUPPLEMENT] 2 99 •j 97 ■■> 99 V 96 •j 92 V 82 Prrreitfat/es of Nutrition in carious Articles of Food. (Moss. Raw Cucumbers................................... f Raw melons......................................... s Boiled turnips....................................— *^ Milk Cabbage......... Currants........ Whipped Eggw Beet*.............. Apples........... Peaches............... Boiled Codfish.....................................£ Broiled venison.................................... ;" Potatoes................................................ *l/i Fried veal............................................. ;J* Roast Poultry. Raw beef................................................ 26 Raw Grapes............................................. 27 Raw prunes............................................. 29 Boiled mutton......................................... 30 Oatmeal porridge................................... 75 Rye bread................................................ 79 Boiled beans............................................ 87 Boiled rice............................................... 88 Barley bread.......................................... 88 Wheat bread............................................ 90 Baked corn brea \.................................... 91 Boiled barley.......................................... 92 Butter ..................................................... 93 Boiled pe>-.t<............................................. 93 Raw oil................................................... 9fi 29/ [supplement] The average percentage of the different food classes needed to sustain a man in perfect health is given in Kensington Museum Handbook on Food: Per ct. Water.............................................-...................... 8i-5 Albuminoids or flesh formers.-.............................. 3.9 starches and sugars....;........................................... 10 6 Fat.......................................................................... 3" Salt (Na CI)................................................................. 0.7 Phosphates, potash salts, etc..................................... 0.3 An Ideal Ration with Solid Food. (Mrs. E H. RICHARDS) Material. Bread .................... Meat............„........ Oysters................ Breakfast cocoa Milk..... Broth...................... Sugar.................... Butter.................... Amount. 453.6 226.8 226.8 28 3 113.4 453.6 28,3 14.1'; 16 8 8 1 4 16 1 i Total........................!....... 106.80 Proteid. Fat. Carb'hydr'tes Grms. Oz. Grms. Oz. Grms. Oz. 31.75 34.02 1.12 1 20 044 0 23 0.13 0.64 2 26 11.34 2 04 7 50 4.42 18.14 12.27 0 08 0.04 0.07 0 26 0.16 0.64 257.28 9.04 0.34 0.17 3.20 0.96 1,206 82 243.72 12.52 70.01 6 60 3 63 18 14 9.60 4 88 90.72 27.36 135.42 75.55 613 21 112 17 0.14 118.62 106.80 57 97 389 84 ........ 2,575.52 The following table i6 a fair average work ration in round numbers, based on such data as those in the other tables: Estimated Work Ration, Maximum and Minimum. Mrs. E. H. RICHARDS.) For one day. Proteid, grammes — — — — — i |:j™ Fat, grammes — — — — — — j ^J* Carbohydrates, gramme's — — — j 7*~ Calories-------------------------{ J,500 About thirty grammes of salts should be added to this [Landois] The bare subsistence ration is much less, as follows: Estimated Life Ration. (Mrs. E. H. RICHARDS.) For one day. Proteid, grammes — — — — — — — 75 Fat, grammes — — — — — — — — 40 Carbohydrates, grammes — — — — — 325 Calories — — — — — — — — — 2.000 [SUPPLEMENT] )0y It will be observed that the totals are somewhat less in this diet than those of the preceeding table, which is designed for a working man who is developing more calories. TABLE OF ENERGY estimated in Foot Tons instead of Calories. (YEO.) Energy developed by one ounce of the following foods when oxidised in the body. Food Stuff. Beef [best quality], uncooked.......... Meat [served to soldiers], uncooked Beef [fattened], uncooked........... Meat, cooked....................__..........____ Corned beef [Chicago].......................... Salt beef...................................___....... Salt pork........................................____ Fat pork___...................________......... Dried bacon.............. Smoked ham...... Whitefish....................................... Poultry.................................. Bread Wheat flour............................................_. Biscuit ...................................................... Rice........_.....................................___....... Oatmeal........................_.......................__ Maize.......................................................... Macaroni... Millet........................................................ A r ro w root................................................ Peas [dried]............................................ Potatoes.................................................... Carrots...................................................... Cabbage.................................................... Butter____........................._.................... Eggs.......................................................... Cheese........._......_...................................... Milk [cow's], new........._.................___ Cream___..........................................._..... Skimmed milk..................................___ Sugar........................................................ Pemmican................................................ Ale [Bass's bottled]„............................. Stout [Guinness]................................... With usual per- centages of water Foot tons. 96.0 102.6 124.0 52,0 71 6 202.0 292.3 179.6 44.3 50.7 87.5 123.6 173.3 126.5 130.0 132.0 122.7 125.9 116.4 118.9 33.0 14.3 13.0 344.5 67,3 149.9 26.9 109.2 20.4 126.4 270.1 30.0 41.5 One ounce water-free. Foot tons. 199 243 280 240 217 138 166 336 346 267 209 204 147 146 189 141 154 160 146 149 138 151 141 137 158 367 265 245 225 365 1S1 128 293 260 360 Prof. Egleston's standard of nutrition is high. He places the daily al- lowance of nutritive material at 700 grammes, divided as follows:— Carbohydrates, 400 grms:—Fat?, 150 grms:—Proteid, 150 grms: yielding in all, 3.650 calorics. y\h | SUPPLEMENT] Percentage Composition of Edible Portions of Garrison Ration. (Captain C. E. Woodruff, M. D. Asst. Surgeon, U. S. A.) Water. ! Protein. Bacon,fat................ Beans........................ Pork, salt and fat...... Sugar, ground.......... Sugar, brown issue.. Flour....................... Beef........................ Potatoes................... Onions...................... Oatmeal ...................... Cornmeal..................... Canned apples.............. Dried apples................. Tapioca or cornstarch... Butter ......................... Syrup........................... Lard............................ Rice............................. Canned corn................ Canned tomatoes.......... Macaroni and vermicelli Milk, fresh................... Milk, condensed .......... Peas............................ Raisins......................... Cheese......................... Prunes......................... Cabbage ...................... Ham............................ Apricots, canned.......... Barley.......................... Chocolate..................... Sausage........................ Oysters ........................ Salmon, canned............ Crabs........................... Crackers......................I 20.0 12.6 12.1 2.0 3.0 12.5 55.0 78.9 s;.o 7.6 15.0 83.2 25.0 2.0 10.5 43.7 12.0 12.4 81.3 96.0 13.1 14.1 25.0 12.3 40.0 35.0 30.0 92.0 41.5 50.0 12.0 41.2 87.1 63.6 8.00 23.10 0.90 11.00 17.10 2.10 1.4 15.10 9.20 0.20 0.90 1.00 6.60 7.4 2.80 0.80 9.00 0.843 17.00 26.70 0.40 33.00 2.50 2.10 16 7 2.00 13 00 20.00 13.80 6.00 21 60 15 0 10.3 Fats. Carbohy- drates. 69 5 2.0 82.8 1.0 27 0 0.1 03 7.1 3.8 0.4 1.8 85.0 59.2 9f 8 96.5 74 9 17.'9 10.1 68 2 70.6 15.9 71.5 97.8 0.5 55.0 83 4 0.4 794 1.1 13.2 0.4 2.5 0.3 76 8 0.802 1 069 11.0 4400 1.7 56 40 24 00 22.0 5,00 12.0 0.6 0.0 39.1 30.0 2.7 76.0 50.0 10.0 42 8 1.2 3.7 13.4 1.0 94 70 5 Salts, ~2.5 3.1 4.2 02 0 5 0.5 0.9 1.0 0.6 2.0 1.4 03 1.4 02 3.0 2.3 4.0 0.4 0.6 0.3 0.8 0.164 3.0 2.9 0.6 5 0 0.6 1.1 2.7 0 6 3.0 40 2.2 2.'6 1.4 Energy Calories per lb. _ 3,080 1,615 3,510 1,820 1,795 1,644 1,460 375 225 1,850 1,645 315 1,418 1,820 3.615 1.023 3.570 1,630 345 80 1,406 418 1.595 1,565 440 1.600 140 155 1,960 460 1,800 2.650 2,065 230 965 526 1,900 Church furnishes the following table showing the number of tons which it is calcu- lated could be raiseed through the height of one foot by the complete combustion of a single pound of each kind of food. In the body only about a fifth of this energy would develope work, the rest going into heat production: 1 pound beef fat " oatmeal '' gelatin " lean beef '' potatoes '' milk " ground rice raises 5,649 tons 1 foot high. " 2,439 tl 2,270 c..... 885 il 618 " 390 " 2,330 " " 25 — tannic acid and alcohol, but erythro dextrin and achroodextrin are precipitated by alcohol and ether, not by tannic acid. These two dextrines do not reduce Fehlings solution and do not ferment with yeast. 3. Maltose:— Soluble in alcohol, insoluble in ether, reduces Fehling's solution, but not Barfoeds reagent [a weak'4 percent sol- ution of cupric acetate to which 1 percent acetic acid is added.] does not ferment with yeast. 4. Dextrose:—Insoluble in alcohol and ether, reduces Fehl- ing's as well as Barfoed's solution; ferments readily with yeast. It is important to familiarize oneself with these reactions as it often becomes necessary to determine in cases of hyperacidity or supersecretion the degree of starch conversion. It was formerly thought that the starch was first converted to dextrin, and this in turn was converted to sugar. According to Prof. W. H. Howell, it is believed that the starch molecule, which is quite complex, consisting of some multiple of C6 HlO O5 — possibiy C6 HlO 05.20 — first takes up water, thereby becomes soluble [soluble starch, amylodextrin], and then splits, with the formation of dextrin and maltose, and that the dextrin again undergoes the same hydrolytic process may continue under favorable conditions until only maltose is present. The difficulty at present is in isolating the different forms of dextrin that are produced. It is usually said that at least two forms occur, one of which gives a red color with iodine, and is known as erythrodextrin, while the other gives no color reaction with iodine, and is termed achroodextrin. It is pretty certain, however, that there are several forms of achroodextrin, and according to some observers, erythrodextrin also is really a mixture of dextrins with maltose in varying proportions. In accordance with the general outline of the process given above, Neumeister pro- poses the following schema which is useful because it gives a clear representation of one theory, but which must not be considerd as satisfactorily demonstrated, [see also the section on Chemistery of the Body.] Starch-soluble starch ( Maltose. Erythrodextrin. \ Maltose. (amylodextrin,) I Achroodextrin. a \ Maltose. \ Maltose. Achroodextrin. b^ Maltose. Achroodextrin ci ,. ., Uiialtodextrin.) I MaltOSC — 26 — Von Mering and Ewald have shown that in the transformation of starch into sugar by ptyalin, the greater portion is converted into maltose, only a small portion into dextrose. But the maltose form- ed in the stomach, is changed to dextrose in the intestine. If the amylaceous transformation proceeds normally in the mouth and stomach, after a time, within an hour at least, so much starch has been changed into achroodextrin, maltose and dextrose, that the ad- dition of small quantities of Lugol's solution to the filtered stomach contents no longer produces any changes in color. The occurence of a purple [erythrodextrin] or a blue color [starch] shows that the sugar transformation has been incomplete. Now this may be due either to a deficiency of ptyalin or to a rapidly increasing acidity or hyperacidity of the stomach. Ewald says that although he tested a large number of patients for the fermentative power of saliva, he never found a saliva that could not convert starch into sugar. This too, when he tested the salivary secretion of patients with dental caries, angina, diphtheria and carcinonia of the tongue. From the above it is evident that there must be two stages of gastric digestion, [1] an amylolytic and [2] a proteolytic. Having satisfied ourselves as regards the fate of the carbohydrates or starches, let us proceed to study proteolytic digestion or conversion of pro- teids, albumens, gelatins, fibrins, elastin, meat, etc. etc. The secretion of the stomach is a complex fluid, clear, colorless, and of acid reaction, it has only >4 per ct. solid ingredients: the amount secreted in 24 hours is about 1600 grms. Its chief constitu- ent is hydrochloric acid which it contains in the amount of 0.1 to 0.22 per ct. (One to two per mille.) This degree of acidity is not reached at once, but gradually; at the beginning and end of stomach digestion, the percentage of HCL is considerably less. Besides the HCL gastric juice contains two unorganized ferments. Pepsin and Rennet ferment. Hydrochloric acid acts in six different ways, all of which are of great significance for the normal progress of digestion. 1. HCL acts as an antizymotic or antiseptic, destroying patho- genic organisms and preventing abnormal fermentations. This anti- bacterial effect extends even into the duodenum. 2. HCL has the power to convert the proenzymes of the gas- — 27 — trie glands, (Pepsinogen and Rennet zymogen) into active ferments in a very short time, according to Langley in one minute. 3, This gastric acid posseses a certain regulatory influence on the progress of peristalsis. 4. HCL forms with the aid of pepsin—albuminous bodies in- to peptones, gelatin into gelatin peptone, elastine into elastin pep- tone. But in reality the pepsin is the main or chief agent in these transformations as the HCL'can be effectively substituted by HNO3—phosphoric, oxalic, sulphuric, lactic and butyric acid. 5. By HCL cane sugar is changed to invert sugar. (Dextrose and Laevulose.) This property is also ascribed to a number of bacteria, that can invert cane sugar although after a longer time. 6. HCL finally is instrumental in bringing the soluble calcium and mognesium salts, introduced in the food, into the solution. Concerning the origin and derivation of ?the hydrochloric acid- we unfortunately have nothing but speculation. No free acid occur- ing in the blood or lymph, it is rational to conclude that it is pro- duced in the secreting [oxyntic] cells of the gland ducts. It seems probable that the acid is derived from the neutral chlorides of the blood, which are in someway decomposed, the chlorine uniting with hydrogen to form HCL. The acid is secreted at the gastric mucosa whilst the base remains behind and probably passes back into the blood. This in a way explains the increased alkalinity of the blood, and the decrease of acidity of the urine after meals — the return of basic substances into the circulation naturally having such an effect. According to Heidenhain a free organic acid is secreted by the cells [oxyntic] which then decomposes the chlorides. According to M aly the HCL is the result of a reaction between the'phosphates and chlorides of the blood as expressed in the following two equations. Na H2 P04 plus Na CI equals Na2 HP04 plus HCL or 3Ca C12 plus 2Na2 HP04 equals Ca3 [P04]2 plus 4Na CI plus 2Hcl. What is known thus far of the specific action of living cells, en- forces the impression here as in other chemical process not yet un- derstood and that is that vital phenomena are difficult to express in chemical formulas. LECTURE "V. PEPSINOGEN AND PEPSIN — RENNET AND RENNET ZYMOGEN — INTESTINAL DIGESTION — DUODENAL INTUBATION. IT SHOULD not be understood that all combinations of the gastric juice with albumens are at once peptones, like the starches these proteids reach their end stage of gastric digestion by four distinct intermediate stages. . These are (1) Globulin, (2) Acid albumin or Syntonin, (3) Propepton or hemialbumose, (4) Pepton. Besides forming peptones out of albumins, pepsin de- prives gelatin of its property to coagulate or rather to gelatinize, and forms gelatin peptones out of it. Peptones are derived from tgg, serum and plant albumens, gelatin, meat, fibrin, casein, etc. No other mineral acids gives as good results with pepsin as HCL which can form pepsin from pepsinogen in the quickest time. It is useful to be able to test for propeptone formation. In normal digestion one hrour after the test breakfast, propeptone is present only in traces, or usually is not to be detected at all, but in abnor- mally slow digestion it is still abundant at that period. The best method up to present date is by means of the Biuret reaction. In this reaction a dilute solution of cupric sulphate is added to stomach contents in the cold, and a few drops of potassi- um hydroxide added sufficient to make the solution alkaline, an in- tense red color results. Cupric sulphate and KOH added to ordi- nary albumen and syntonin, without warming produces a bluish violet, which must be distinguished from the purple red of biuret. The more marked the propeptone. reactions are, the less the — 29 — peptone which has been formed and eventually removed rfrom the stomach. We can approximately estimate the amount of peptone by the intensity of the biuret reaction, if we always use the same quantities of stomach contents, caustic potash and cupric sulphate and compare it with the reaction given with a peptone solution of known strength. Peptone gives the same pink, purple red-color with the biuret reaction as propeptone. If we desire to estimate the rate of proteolysis in the stomach, the biuret reaction will not per- mit us to distinguish between these two bodies, the only differen- tiation possible is by precipitation of the propeptone, in the follow- ing manner: The stomach filtrate is carefully neutralized an equal quantity of common salt solution is added and then a few drops of concentrated acetic acid. A precipate will be propeptone which can be filtered off and weighed; any red biuret reaction after this sepa- ration must be due to peptone. In order to determine in a given specimen of stomach contents whether the pepsin or HCL is present in too great or too small a quantity, one proceeds in the following manner:— Pour 10 c.c. filtered stomach contents into four test tubes and number them Nos. 1.—2.—}.—4. To No. 1. nothing else is added: to No. 2. enough HCL to make a solution of 3 to 5 per mille. (This can be accomplished by adding one to two drops of officinal HCL U. S. Pharm. to 10 c.c. filtrate.) To No. 3, 0.2 to 0.5 grammes (gr. iii to gr. vii) of pure pepsin is added, and to No. 4. both HCL and pepsin are supplied. A small disk of egg albumen, (which is prepared by cutting boiled egg albumen into lamellae of uniform thickness with a mi- crotome and punching out equal circles by acorkborer) is added to each test tube and they are then put in the thermostat incubator at 100°. The rate at which the albumen is dissolved will tell us whether the filtrate was perfect in the requisite amount of pepsin and HCL, whether pepsin alone or HCL only or finally whether both were necessary. In this way we can discover which factor is at fault. In the human stomach the formation of peptone remains at a certain percentage by the removal or absorption of peptones over that amount, and also it would seem by an inhibiting influence which a certain percentage of peptone has over the proteolytic pro- cess in retarding or suspending it. As this cannot be imitated in - 30 - a test tube, i. e. the absorption of ready formed peptones, a seem- ingly delayed digestive process of egg albumen disks in the test tubes may in reality be due to a very active stomach filtrate. (Ewald.) Rennet is the second gastric ferment which produces a light, not very cohesive coagulation of milk. This coagulation is a char- acteristic cake of casein floating in clear serum, more-dense, not lumpy, more cohesive coagulation than produced by acids. This ferment is a constant constituent of the stomach contents just as pepsin and pepsinogen. With a complete absence of the rennet, one can with certainty conclude that the case is one of atrophy of the gastric mucosa. The demonstration of rennet ferment is carried out in the fol- lowing manner:— 10 c.c. of raw, unboiled milk are placed in the incubator with 2-5 drops of stomach filtiate. If rennet is present the characteristic milk coagulation will occur in a variable time. (1 minute to several hours, according to quantity of ferment.) Occasionally rennet, the perfect ferment is not contained in the stomach contents whilst at the same time, rennet zymogen is present. This is demonstrated according to Hammersten by adding to the mixture just described 2 c. cm. of a concentrated solution of calcium chloride CA CL2. If a rennet coagulum occurs it follows that rennet zymo- gen is present but not the perfect ferment. For these tests, raw milk only can be used, as it coagulates 10 times as rapidly as boiled milk. Jaworski has pointed out that in cases where tests for rennet and rennet zymogen are both negative, it is advisable to try pouring a 0.3 to 0.6 hydrochloric acid solution into the stomach to see whether this HCL may not be able to awaken a secretion of rennet; this should be done especially before making the diagnosis of com- plete atrophy of the mucosa. The PHYSIOLOGY of INTESTINAL DIGESTION. Our knowledge of the digestive processes in the intestine, is from a physiological as well as from a pathological point of view defective, at times contradictory. Concerning gastric digestion, we are rrmch better instructed because here the processes are simpler and material for investigation can be more easily obtained. The stomach tube supplies us without difficulty with gastric contents, - 31 — but hitherto all intestinal contents of human beings have been ob- tained from rare cases of intestinal fistulae, for the faeces give no information of the digestive actions in the smaller intestine, that are constant and reliable. The earliest investigations of intestinal contents were made in 1662 by Regnier de Graaf, who made experimental fistulas into the intestinal canal of animals. It is a curious historical fact that this intestinal experiment antidated the first investigations of stomach contents which were carried on in 1752 by Reaumur. So up to the present time there was no prospect of getting a better insight into the physiology of intestinal digestion; until a method for intubating the duodenum in the living human subject was devised by myself. This method which is described in the Johns Hopkins Hospital Medical Bulletin for April 1895, and also Boas' Archiv for Digestive Diseases, Vol. II, page 85, consists of the introducton of a thin elastic rubber bag into the stomach. This bag when folded over a tube which runs through it does not occupy as much space as an ordin- ary stomach tube, and has the exact shape of the human stomach - 32 - when it is distended by blowing'it up within that organ, whereby it fits itself exactly to, and is closely applied to the gastric walls. The intra-gastric bag is distended by the pressure apparatus shown in figure 4. The graduated bottle (A) is full of water and elevated above the bottle (b) which is empty and also graduated. The stomach shaped bag, (c) when it reaches the stomach is connected with the lower empty bottle, (b) Then the stop-cock permitting the water to run from A to B is opened, and the water runs from A into B displacing the air in B which distends the bag c within the stomach, filling it entirely. As you can observe on this bag, a guide is contained in it, running along the dotted line paralell to the lesser curvature. In this guide the duodenal tube is inserted, lubricated with oil before the bag is pushed into the stomach. This tube is provided with very thick walls, by virtue of which it is not easily kinked or bent upon itself. The relation of the thickness of the walls to the diameter of the Jumen is shown in the crossectfon of figure 2. When the intra-gastric bag is blown up, if fills the stomach entirely. The duodenal tube - 33 - lies in its sheath or guide, and, on pushing onward from the mouth, it is not possible for it to go anywhere else except through the py- lorus into the duodenum. In the figures it can be seen that the bag is not distended by the duodenal tube, but a separate, very small tube runs down the oesophagus, ending in the bag, serving the pur- pose of its distension. Both tubes together do not occupy as much space as an ordinary stomach tube. A description of this method seemed essential because, it seems to be destined to bring our knowledge of the physiology and path- ology of the intestines upon a basis of ascertained facts. Because we can at any time, thereby obtain the contents of the intestine, the gut may in any of its parts be reached with safety. After known test meals it is possible, after they have passed from the stomach into the duodenum, to draw out samples from this part and subject them to analysis. By alternately distending any part with air or water, we will be enabled to locate the part by the percussion sound on the outside of the abdomen, and the dis- tance it is located from the mouth can be seen from the length of tube introduced. Small electric lamps may be introduced into the duodenum as they are into the stomach, and, the location and condition recog- nized by electro diaphany. In all experiments on this subject hitherto, it has been impossi- ble to obtain either the pancreatic or biliary secretion in a pure condition; this is due to the fact that both the pancreatic and the common gall duct empty into the descending portion of the duode- num very near each other. Just at present I have under observation a female patient who has suffered repeated biliary colic. At times she passes small stones without giving her much pain, at least they are found in the stools without having given her any colic. She is willing to undergo an operation to be relieved. Through the comparitively thin abdomi- nal walls I am able to feel numerous stones in the gall bladder. She consented to an attempt at intubation of the duodenum to deter- mine whether there was any bile secreted. The duodenum was en- tered without difficulty and cleansed by running in and aspirating out destilled warm water. Twentyfour hours afterward the duo- denum was again intubated according to my method, and washed ■ H with 100 c.c. of warm distilled water. On being aspirated this water was still clear but viscid and sticky, similar to a solution of egg albumen. It contained no bile pigments nor cholestrin, and was free from taurocholates and gly- cocolates. It was colorless and odorless and seemed very rich in some form of albumen. That it was pure pancreatic juice was pro- ven by its digesting fibrin and serum albumen. The juice obtained in this manner will digest from 85 to 95 per cent of Merck's dried serum albumen in the digestorium at 100° F. in 2 hours. The Amylolytic and fat decomposing property of the juice was determined in a similar manner. One is therefore justi- fied in concluding that in this case the pancreatic juice was obtain- ed almost pure as there were no bile elements cpntained in it; the bile being prevented from entering the duodenum by a calculus or catarrhal occlusion. As there are also pancreatic calculi, or occlu- sions of the duct by neoplasm or catarrhal swelling, it is conceivable that we may yet be able to obtain the bile in a pure condition, and free from pancreatic juice in the human subject. The secretion of Brunner's and Lieberkiihns glands will how- ever always constitute an admixture of these juices. The PANCREAS; its SECRETION and PANCREATIC DIGESTION. In 1846 Claude Bernard made the first scientific and funda- mental investigation concerning the pancreatic secretion. Later on Kiihne, Bidder and Schmidt, Corvisart, Haidenhain and others en- larged these results. Its secretion as Bernard first observed is dependant upon diges- tion and is a clear colorless and odorless fluid, very alkaline and so rich in albumen that it solidifies on boiling. Zawardsky had oppor- tunity of analyzing the normal human pancreatic secretion in a case of pancreatic fistula, which remained behind after removal of a tumor. According to his analysis it contained 86.4 percent water, 13.25 organic substances; among the latter are 9.2 proteid bodies and O.83 extractive substances soluble in alcohol, lastly 0.34 perct. salts. The chyme which passes into the duodenum from the stomach comes under the influence of formed or organized and unformed - 35 — or unorganized ferments. The formed and organized ferments are represented by bacteria which bring about 'carbohydrate fer- mentation mostly in upper, bowel and proteid putrefaction, mostly in lower bowel. The unorganized ferments are contained in the pancreatic se- cretion, the bile and in the succus entericus. The most important constituents of the pancreas are three ferments or enzymes. [1 ] An Amylolytic, [2] a Proteolytic, [3] a fat splitting ferment. According to W. G. Halliburton and T. G. Burton, (Journal of Physiology, Vol. XX, page 106.) pancreatic juice possesses a milk precipitating substance, causing at 35°-45°c a granular precipitate in milk, but there is no solidification until the milk cools, when it sets to a coherent curd. On warming, the curd is broken up, the milk resumes its granular fluidity. The granular precipitate pro- duced by pancreatic juice, seems according to these observers to be intermediate between casein and caseinogen. . The amylolytic or pancreas diastase is very similar to ptyalin in its action, and changes boiled starch into maltose exceedingly rapidly at body temperature. In addition, small quantiies of dextrin and grape sugar are formed; one gram of pancreatic juice from a dog will invert 3.6 grams starch into sugar. Cane sugar and inulin are not affected by it. According to Zweifel, this ferment is absent in the pancreas of new born children. The fat splitting ferment of the pancreas, (also called steapsin) which thus far has not been obtained in a pure state, breaks up neutral fats into fatty acids and glycerine.. This process occurs very slowly however;—Berthelot found that 15 grams of pancreas secre- tion of the dog required at least 24 hours to break up 2 decigrams of monobutyrin completely into butyric acid and glycerin. The fatty acids formed during this transformation, combine with alka- lies in the intestine to form soaps, which by emulsifying other fats assist greatly in their absorption. In the laboratory it always re- quires powerful mechanical action to effect an emulsion of fats, not so in the intestine, where it is evidently accomplished with great facility. That this must greatly assist in fat resorption is evident from the frequent observation that after the disease of the pancreas the feces becomes very rich in fat, which may be present in such a large amount as to congeal on the surface oi the stool. - )6 - The proteolytic ferment of the pancreas has been called trypsin by Kiihne. Using pancreatic juice and boiled blood fibrin, he found that it did not swell up, but that it became very fragile, and finally liquefied. As we take in all of our albumen in a boiled or roasted state, which becomes peptones in the stomach and not soluble albu- men, the question has arisen—where do we derive our soluble native albumen? This is obtained from pancreatic trypsin digestion of boiled albuminous bodies, which changes them to albumen soluble in water or at least in weak saline solution from which they can be precipitated by heat. The proteolytic action of trypsin, takes place in an alkaline or neutral medium only. Among the bodies formed from albumens and proteids under the influence of. trypsin are a glolulin that is insoluble in water, hemi and anti-pepton, leucin, tyrosin and asparaginic acid. Indol, which is found in the jejunum is a product of bacterial action on albumens. A chromogenic body has been described by Tiedeman and Gmelin which has received the name tryptophan, it is a» result of extensive albumen decomposition. Trypsin, then to sum up, changes proteids to peptones and soluble albumens, casein to casein- peptones, gelatine to gelatoses and gelatin-pepton, and, elastin to elastoses and elastin-peptones. In animals that have been deprived of their pancreas by opera- tion only 44^ of proteid, 57^ to 70fc of carbohydrates and no fats at all were absorbed, although four-fifths of the fats were split up into fatty acid and glycerin. LECTURE VI. The BILE — The SUCCUS ENTERICUS — INTESTINAL FERMENTATION — PUTREFACTION — FORMED OR ORGANIZED FERMENTS. IT IS KNOWN at present that the bile exerts no chemical effects upon the food materials, nevertheless its presence in the duoden- al chyme is significant on account or its alkaline reaction and its effect on the mucous membrane. The most important function of the bile is the excretion of metabolic products that cannot be utilized. The contents of the gall-bladder represents a concentrated se- cretion, therefore our knowledge of the physiological action of the bile depends upon the discharge of biliary fistula. The bile is a golden yellow, at times olive brown secretion; it is never of a green color, but generally very mucoid and stringy. Its alkaline reaction is due mainly to carbonates and phosphates. The quantity poured into the intestine is largest in the first hour after food is taken. Albumens increase, fats diminish this quantity, whilst sugar and carbohydrates appear to exert no influence. (Voit.) The quan- tity secreted in 24 hours averages 5-600 c. cm. (Ranke, Wittich, -: J 8 Hammarsten.) The quantitative annalyses of Hammarsten have given the following results: Solid materials 1-62 — 3-52 Water 96.47 — 98.37 Mucin and coloring matter 0.27 — 0.91 Compounds of bile acids & alkalies 0.26 — 1.82 Taurocholate 0.052 — O.203 Glycocholate 0.204 — 1.61 Fatty acids 0.024 — 0.136 Cholesterin 0.048 — 0.160 Lecithin 0.048 — O.O65 •Fat 0.061 — 0.095 Soluble salts O.676 — O.887 Insoluble salts 0.020 — 0.049 At times a diastatic ferment fs present in the bile, but it is not a specific constituent (Neumeister) but appears in the bile like the diastatic ferment appears in the urine; it seems to be indentical with the ptyalin zymogen of the urine. When the bile is prevented from entering the intestine at all, albumens, gelatines and carbohydrates are absorbed in a normal manner. (Voit and J. Munk.) But the digestion of fats is very seriously interfered with; a normal animal resorbes 99^ of fats if not more than 150 to 200 gr. are given i. e. only 1 i appears in the feces, but on producing an experimental fistula conducting the bile outward, 60$-of the fats are not utilized. (Voit.) The subjoining is a synopsis of the uses and functions of the bile: 1. Fats are brought into a fine, permanent emulsion by bile just as by pancreatic juice. 2. Bile assists the fat splitting effect of pancreatic juice. (Nencki.) Without bile only 61$ of tribenzoicin were decomposed by pancre- atic juice, with bile the total amount. 3. By its alkalinity it necessitates the formation of soaps. 4. Bile dissolves fats in minute quantities. 5. Bile dissolves the saponified alkaline bases which are insolu- ble in the juices of the intestines. 6. Animal membranes moistened with bile are more permeable to emulsified fats than membranes moistened with water. (v.Wisting Heidenhain. - 39 - 7. Bile is a stimulant to the intestinal epithelial cells, incites their proper functioning and maintains it. (Rohmann.) 8. It is claimed that albuminous bodies and pepsin disolved in the chyme are precipitated as a resinous sticky deposit which adheres better to the duodenal wall and effects a better utilization of the albuminates thereby. 9. An inhibitory influence over putrefaction is ascribed to bile (Maly and Emmerich.) 10. An influence favoring an increase of the peristalsis of the intestine. (Rohmann.) THE SUCCUS ENTERICUS. The succus entericus is a secretion of the crypts of Lieberkiihn and was first studied in man by Demant after a herniotony. This secretion has the color of light rhinewhine and is very strongly al- kaline owing to a percentage of 1.5^ carbonate of sodium. The principal constituents are albumens and mucin. It contains also ptyalin and an inverting ferment, and has no offect on albumens and fats—its purpose seems to be probably that of a neutralizer of the acids originating from fermentation of carbohydrates. For the onward movement of the bowel contents, its excess of mucin may be instrumental. The FORMED or ORGANIZED FERMENTS. — (Bacteria.) Proteids, carbohydrates and fats are subject to decomposition in the intestines by bacteria. Fats are not decomposed to any con- siderable extent in the lower intestinal sections (Nencki and Blank) but a small fraction is split up into glycerin and fatty acids. A greater interest attaches itself to the fermentation of carbo- hydrates, occuring in the upper small intestine principally and lead- ing to the formation of acetic, lactic, butyric acid and alcohols, carbonic acid and hydrogen. It is not known how much of the carbohydrates is decomposed in this manner. The putrefaction of proteids, caused by certain bacteria of the lower bowel only occurs in an alkaline medium. The first products of this putrefaction are the identical bodies which are formed dur- ing pancreatic digestion—viz: albumoses, peptones, amido acids and ammonia, but then the putrefaction goes still further, tyrosin is 40 - formed, and from this, through a series of complex, oxyacids—the product phenol (carbolic acid) is reached, which may yield phenyl propionic and phenylacetic acids. A second variety of aromatic substances, not derived from tyrosin, is represented by indol, skatol and skatol carbonic acid, finally leucin and ammonia salts of capron- ic, valerianic and butyric acids. The gases formed are carbonic acid gas, hydrogen, hydrogen sulphide and methylmercaptan. We cannot measure the intensity of carbohydrate fermentation, but the aromatic end-products of proteid putrefaction can be quan- titatively estimated by the combined and ethereal sulphates occur- ing in the urine. The number of bacteria increases from the duodenum on down- ward until they become enormously prolific in the colon. They differ qualitatively also; in the small intestine, Gessner found a prevalence of the bacterium lactis aerogenes and streptococcus pyogenes, the colon bacillus was present but insignificant in num- bers. In the colon however, the reverse was the case.----It was formerly an accepted view principally defended by Pasteur, that the intestinal bacteria were absolutely indispensable for digestion and therefore for the nutrition of the individual. From this view we have returned to what seems a more logical belief based on ob- servations of Escherich who held that bacteria contribute very little to the nutrition of the infant, as they do not effect casein and fats, but only sugar of milk. [Turning it into lactic and carbonic acid and hydrogen.] The work of Nuttal and Thierfelder shows that guinea-pigs can live on absolutely sterile food. Macfadyen, Nencki and Sieber arrived at a similar conclusion in their now classical observations on adults. [Archiv f. exp. Path- ology, Band xxvm, 1891. One of their objects of study was a fe- male with a fistula that opened the small intestine on the external abdominal wall, just at the end of the ileum. The entire colon was therefore excluded from the digestive act, as all proteid putrefaction occurs in the colon, this case presented a chance to study the absence of products of albuminous putrefaction and its effects. They concluded that bacteria are not at all essential to digestion, as their patient was very healthy without proteid putrefaction. They declare that the bacterial fermentation of carbohydrates in the small bowel as detrimental rather than advantageous inasmuch as the _ 41 bacteria live at the expense of the ingested carbohydrates, therefore a corresponding amount of food is lost to the organism. Our knowledge of the bacterial activity in the intestines, though much enriched by valuable researches in the last decade is according to my opinion in its infancy. So also our knowledge of the patho- genic significance of intestinal bacteria. There is undoubtedly a kind of interaction and correlation between digestive ferments and juices on the one hand and bacteria on the other, or even between bacteria and bacteria, or between the products of bacterial metabol- ism. For instance, Metschnikoff has demonstrated that the multi- plication of the cholera vibrio is much advanced by the presence of torulas and sarcinas in the intestines. It is conceivable that bacteria wage war upon each other as well as upon our cells, and, that we are benefited by this mutual self- destruction of our parasitic inhabitants. It is conceiveable also that that they fall preys to the poisonous metabolic products of their own or other species of bacteria. Certain very decomposable food as cheese, that was rich in germs, has been found by competent ob- servers to reduce the amount of indican and the ethereal sulphates in the urine. The human stomach must not be regarded as an organ that can absolutely sterilize all food. The spores being more resistent to Hcl than the fully developed bacteria themselves, pass through the stomach uninjured. Miller assumes that at the height of digestion only, when the amount of HCL is greatest, the less resistant bacteria are killed, Bunge some years ago announced that the sole object of the Hcl was one of sterilization. It is undeniable from recent in- vestigations, that the human stomach is at no time free from germs. Captain and Morau found them at the height of digestion. Abelous found them in his own stomach when it was perfectly empty. Miller demonstrated that the mouth contains large numbers of microbes, in one unclean individual he estimated the numbers of mouth bac- teria at 1 140000 000. Of 25 different varieties occuring in the mouth this observer was able to demonstrate 12 of the same in the feces. Nevertheless the mouth bacteria according to Lucksdorff constitute only 3$ whilst those entering through the food constitute 97$ of the bacteria of the intestine. There is no autochthonous vegetation of bacteria in the intestine, they are all introduced from the mouth - 42 - or in the food, or reach there by way of the circulation. (Autoch- thonous bacteria means—such as are formed where they are found.) From observations made up to the present time it seems prob- able, that catarrhal and other inflammatory diseases of the intestinal mucosa are not produced by specific, constantly recurring microbes: but that a large variety and many kinds of bacteria are capable of producing these diseases under conditions which are thus far not perfectly understood. It appears furthermore that the same bacterium may at one time be perfectly harmless, or it may cause a light, trivial affection or thirdly a very serious disturbance. This is the case with the bacterium coli communis, which is borne without detriment by the majority of mankind, but occasionally.it is demonstrated as the producer of colitis, Dyssentery and Cholera nostras. The manifold forms of the catarrhal inflammations are explica- ble by the fact that the intestinal flora is very manifold also. These same bacteria are factors in the etiology of diseases of the peritone- um and of all organs that are in connection with the intestines. Even remote organs, not in anatomical connection with the bowel are not safe from their invasion. They are known to gain entrance into the blood and lymphatic channels through losses of substance in the intestinal mucosa. The experiments of Posner and Lewin have taught us that even without such portals of entry they seem to be able to pass through the bowel wall in masses and threaten the organism. Great harm can be done to the general organism, and to special organs in partic- ular not from this invasion only, but also from absorption of the soluble products of bacterial metabolism and of food decomposition. This condition of self-poisoning from toxic substances in the individuals own intestinal canal is spoken of as intestinal autoin- toxication. Not all autointoxications are of intestinal origin — diabetes mellitus for instance is an autointoxication by grape sugar which is in this case a product of disturbed metabolism and does not originate from the digestive canal. The dangers which threaten the general organism from the in- testinal bacteria have given rise to many efforts to sterilize the digestive tract by means of so called antiseptics. Most of the agents used for this purpose — (Calomel, Salol, Naphthalin, Beta- - 4 J — napthol, Bismuth, Creosote, Bismuth, Salicylate) are themselves toxic and in doses sufficiently large to reduce the number of bac- teria to any considerable extent they are harm ful to the body. The putrefaction of proteids as measured by combined and ethereal sul- phates in the urine can only be temporarily diminished by this method Intestinal disinfection is therefore an unsolved problem. Efforts in this direction should still be encouraged, because we may be able thereby to attenuate the pathogenic inhabitants of our insides and render them less virulent. The best disinfectant of the human in- testine is its normal action, and the best way to control putrefaction is by selection of adapted, appropriate diet, fresh air, moderate exer- cise, good sleep, pure water, avoidance of overeating, overdrinking and of chemicals. .LECTURE VII. The EFFECTS OF CONTEMPORANEOUS ACTION OF SEV- ERAL DIGESTIVE SECRETIONS -- QUALITATIVE AND QUANTITATIVE METHODS FOR TEST- ING the MOTOR, SECRETORY and ABSORPTIVE FUNCTIONS OF the STOMACH. HEN THE GASTRIC chyme enters the duodenum, the albuminoid and proteid foods appear partly as syntonin, albumoses and peptones, and partly unchanged. The carbohydrates appear either as erythrodextrin, achroodextrin or maltoses, and partly unchanged. The fats are unchanged; rarely are they found split up—so that one can detect rtaces of fatty acids. Water, according to the interesting investigations of v. Mehring, is absorbed only in very small quantities from the stomach; it appears that fully 99^ of all water taken into the stomach is passed into the u/ 44 — duodenum;—alcohol and whatever is in solution in it, is absorbed readily. Grape, milk and cane sugar, also maltose are absorbed in moderate amounts when they are in aqueous solution; when they are in alcoholic solution, larger amounts are absorbed. Dextrin and pepton are also taken up from the stomach but in smaller quantities than sugar. The amount of the substances resorbed increases with the concentration of the solution. Simultaneous with this resorp- tion a more or less active excretion of water occurs into the stom- ach. This excretion of water into the stomach increases or dimin- ishes as the quantity of substances resorbed or taken up increases or diminishes. Excretion of water occurs even when no HCL is demonstrable in in the stomach. The chyme, as it enters the duodenum then, still contains all of its water but is minus some of the peptones, dextrins, sugars and alcohols. It is more or less acid from free Hcl, when the bile acts on this acid chyme a resinous flocculent precipitate is depos- ited from it on the walls of the duodenum, at the same time a finely granular cloudiness occurs. The resinous deposit consists of bile acids and syntonin (Hammarsten), and the granular opacity is due also to bile acids and small amounts of peptone. Excess of bile may redissolve these precipitates'so that they can not at times be found in animals killed at the height of digestion. The digestion by pepsin is checked by the complete neutralization of Hcl by pancreatic juice, bile and succus entericus. If any precip- itation occurs as stated, pepsin is also thrown down and resorbed again. The bile does not disturb the proteolytic power of pancreatic juice (Claude Bernard.) Boas and myself have shown thatduode- nal chyme will digest 81$ serum albumin in 3 hours at 40°c. its al- calinity was 0.8$0 Na2 Co.,. He also showed that this duodenal chyme converted 25$ starch into maltose in 3 hours and that it produced 12.1$ fatty acids from neutral olive oil in 3 hours. Boas obtained his mixture of bile pancreatic juice and succus entericus, from a patient who had most probably a duodenal stenosis and vomited this chyme frequently. In my experiments, the duodenal chyme was obtained by my method of intubation of the duodenum. It was found in my experiments that the duodenal juices, when filtered digested 85$ to 95$ of Merck's dried serum albumen in 3 hours at 40°c. My results with starch conversion show that the — 45 - filtered duodenal juices will digest 42$ of starches or rather convert them into maltose which is considerably in excess of the figures ob- tained by Boas. The fat splitting effect observed by me in this juice was again more near the result of Boas, for in my experiments 15-3$ of fatty acids were obtained from neutral olive oil. In a case of billiary calculi, I have been able to obtain the pancreatic juice free from bile as the bile ducts must have been stenosed; either by a small calculus or a bit of thickened bile and mucous mixed. The fat splitting effect of pancreatic juice is improved by the presence of bile, as is also the amylolytic action of amylopsin. (Demonstration)—You have an opportunity here of studying the ac- tion of pancreatic juice on neutral olive oil 10 c.c, and also on starch 10 e.g. in distilled water. This pancreatic juice was obtained from a dog in pure state by putting a canula in the pancreatic duct. I will arrange two test tubes, each with neutral oil, but add 10 c.c. of bile to one only; the other contains simply panceatic juice; then 2 more test tubes are arranged, each with a known quantity of starch; say that 10 e.g. of starch are added to each, in one is contained only pure pancreatic juice, in the other pancreatic juice with bile. Now we will place these four test tubes; two with pancreatic juice only and neutral oil and starch respectively, and two with pancreatic juice plus bile and oil and starch in each respectively in the incuba- tor at 40°c. for 3 hours, and, tomorrow you can determine the amount of oil split up in the test tubes containing it and convince yourselves that pancreatic juice plus bile will split up more fat than without it, and that it will convert more starch into maltose with bile than without it. (Martin and Williams.) Trypsin has no effect on pepsin, but in an acid solution, pepsin is claimed to check the action of trypsin. (Kiihne, Langley, Ewald and Baginsky.) The ferment action of bacteria in the small intes- tine is limited to the carbohydrates. Discharges of food from fistula of the small intestine show no foetid decomposition of albuminoids (Ewald and Nencki.) The absence of proteid putrefaction in the small intestine is probably due to the rapid downward movement of the food mass in this bowel portion and to the acid condition. Carbohydrate fermentation yields mainly lactic acid, aethyl alcohol, carbon dioxide and hydrogen. Macfadyen, Nencki and Sieber found that the chyme that passed over into the large intes- 46 tine, the coecum, from the ileum to be 550 grs. with 4.9$ solid residue in case the chyme was of a very thin consistence, and 232 grs. with 11.23$ solid residue if the chyme was very condensed. Both of these figures are the amounts passing in 24 hours, the shortest time in which food passed into the coecum after it was swallowed was 2 hours, the longest period $% hours. The reaction expressed in acetic acid was equal to 1 pro mille; the acidity is considered to be due to acetic acid, as the lactic acid and the HCL is neutralized by the succus entericus. This chyme contained 1$ albumen, pepton mucin, also dextrin and sugar, also lactic acid, sarcolactic acid and traces of fatty acids; it contained no leucin, tyrosin, urobilin, nor ammonia. This chyme contained none of the characteristic products of albuminoid decomposition. Jakorwski's investigations on the con- tents of the large intestines that were discharged from a fistula in the ascending colon, showed that the daily fecal discharge of 150 - 200 gr. was decidedly alcaline and contained the products of proteid and albuminoid decomposition;—viz urobilin, skatol, phenol, oxy- acids, ammonia, leucin, cadaverin, aethyl and butyl alcohol sul- phuretted hydrogen and methyl mercaptan. In view of the fact that the putrefaction of albuminoids and proteids occurs mainly in the colon, it is of interest to know how much of this class of food substances is left for the colon and how much is digested in the small intestine. Nenki found that when the food contained 70.74 grs. albumen which represents 10.602 grs. nitrogen —the amount of solid material discharged from a colon fistula in 24'hours was 26.5 grs. with 1.61 grs. nitrogen which rep- resented 10.06 grs. albumen. From this it is evident that 14.25 $ or in other terms only one seventh of the total albumen is left for the digestion in the colon, and that 85.75 $ are resorbed from the stomach and small intestine. The intensity of putrefaction in the colon depends upon four factors: (1) The amount of decomposable albuminoid material in- gested. (2) The duration of their retention in the colon. (3) The vigor and tonicity of the intestinal peristalsis and lastly (4) the chemical reaction for a very strongly acid reaction due to free acids inhibits putrefaction. Bile assists in this inhibition. Hirschler has demonstrated that - 47 carbohydrates suppress putrefaction considerably which is due to the lactic, butyric, acetic, and carbonic acid caused by their fermenta- tion. Albumen and pepton are absent from the contents of the rec- tum (feces) but are present in typhoid fever (v Yaksch) pepton is found also in all diseases that may produce pus in the evacauations for instance dyssentery, tuberculous intestinal ulcers, perforation, pertonitis, hepatic cirrhosis and carcinoma. A very important inquiry is that into the ultimate fate of the digestive ferments; do they pass through the entire intestinal tract? are they absorbed or are they decomposed or do they appear in their active form in the feces. This question is a very difficult one to solve, as our only methods of detecting pepsin, trypsin, and ptyalin for instance is by their digestive activity. In all experiments of this kind the feces must be first sterilized by saturated solutions of Thy- mol, before using this it is well to exclude the action of peptonizing bacteria by removal of these by filtering through a Pasteur filter. If we found in the glycerin extract of the sterilized feces a substance which would dissolve boiled egg albumen in a solution of 0.2$ HCL we should be justified in concluding that it was pepsin. If it did not digest in HCL but in a .1$ solution of sodium carbo- nate it would probably be trypsin. For the demonstration of a diastatic ferment a dilute solution of starch is brought into the incubator with about 5 c.c. of glycerin extract of sterilized feces. After a few hours the HCL and soda solution of the boiled albumen is tested for pepton by the biuret reation and the diastatic test tube is tested with a dilute solution iodide of potassium, if the starch is unchanged the solution will be changed to blue, if not, the color will be brown or yellow. The digestive action of the succus entericus which according to Griitzner has a weak fibrin dissolving property, does not extend to , the albumens and therefore it will not confuse the result stated a- bove as pertaining to pepsin and trypsin. The chief digestive action of succus entericus is on the carbohy- drates. If pepton occurs in the stools it is in my opinion a product either of pepsin or trypsin digestion, not of bacterial origin. Un- doubtedly there are proteolytic bacteria, for instance the bacillus sub- tilis of Ehrenberg the proteus vulgaris of Hauser, the bacillus pu- trificus coli of Bienstock and the bacillus liquefaciens ilei Macfadyen _ 48 — Nencki and Sieber, all of which exist ordinarily in the human in- testine, and their first products of action on albumens are the same as occur in normal pancreatic digestion - viz. Albumoses peptones amido acids and ammonia, but then the action continues uninter- uptedly to the production of decomposition bodies stated in previous lecture. The bacterial produce of peptone is probably of no use to the organism in which it occurs, as bacteria do not make peptone for any philanthropic reason, but because it is a first stage to pro- teid putrefaction and possibly because these proteolytic parasites need peptone for their own existence. The remote possibility that bacteria could produce peptone in the colon (feces) might be excluded by the fact that after steriliza- tion of the feces by a saturated solution of thymol: peptone will in some cases still be produced when above tests are made — more often will this be due to pepsin as it occurs only in an acid medium during the testing, but rarely it is due to trypsin which is present only in the stools where they have traversed the intestines rapidly. Starch inverting ferments are present in the saliva, pancreatic juice and succus entericus, hence if such a ferment appears in the feces it is impossible to conclude its source. Amylopsin and steapsin have as such not been demonstrated in normal feces. Pepsin and rennet occur in normal feces. Person- ally I have found a proteid dissolving ferment in the stool which acted in a \$ solution of carbonate of sodium only, and was stud- ied in a case of complete atrophy of the gastric mucosa, with total absence of Hcl, pepsin and rennet, and also the proenzymes of these ferments. In the wash water bits of mucosa were found that proved the absolute destruction of the glandular apparatus of the stomach. It is probable that this ferment was trypsin, there was a mod- erate gastrectasia, but otherwise no anatomical defect observable. The stools were not diarrhoeic. Escherich's assertion that the colon bacteria do not live upon the food introduced; as according to his opinion, there is no digestibls food left thers under normal con- ditions, but that they live upon the secretions of the walls of the colon is certainly — if this statement of his view is correct—(Man- naberg in Nothnagels Erkrankungen des Darms, p. 38.) erroneous. The conception of some writers on this subject, that food ma- terials are completely used up in the digestive tube, is not proven — 49 — by actual fact. Even meat when eaten in a most digestable form is found undigested to a small extent in the evacuations. It is there- fore more than probable that the colon bacteria live at the expense of the ingested proteid food. Having thus far reviewed the physiology anatomy and in parts the pathology of food digestion in general, let us now return to the special pathology of the functions of the stomach as a preparation for a better comprehension of its diseased states. QUALITATIVE AND QUANTITATIVE METHODS FOR TEST- ING the MOTOR, SECRETORY and ABSORPTIVE FUNCTIONS OF the STOMACH. The motor or peristaltic function is the most important one, because a man may be able to live without the secretory and resorp- tive function of his stomach as the intestinal digestion and secretion would suffice for the conversion of carbohydrates and proteolysis and one depends upon the small intestine for the digestion and absorption of fats altogether, So that even in the total absence of gastric resorption and the falling away of secretion of HCL, pepsin and rennet ferment; life could be maintained" But if the motor function is interfered with the food would re- main in the stomach, and accumulate. If a normal gastric juice were even possible when the peristalsis is paralyzed, the food could be only partly digested. Carbohydrates and fats would not be di- gested. When the limit of distention was reached the food would be ejected (Pyloric Stenosis Gastrectasia.) In all cases of inhibition or loss of motor power the secretory power is seriously disturbed or may cease absolutely so also the re- sorptive power. Many cases of total absence of gastric secretions have been reported — (in fact 1 have shown you a colored patient in the clinic in whom this is the case and yet he is gaining weight on carefully selected diet) in patients whose body weight continued normal and their general health unimpaired. The stomach has been removed experimentally in dogs and the animals continued to thrive without it. There have been up to very recently six different methods pro- posed for determining the motor functions of the human stomach. -— 50 — The methods of Leube, Ewald and Sievers, Klemperer, Fleischer, Einhorn and Hemmeter. Leube's method of estimating the duration of digestion i. e. to determine after a definite average time of six to seven hours after a meal of 50 grs. bread - 200 grs. beefsteak and a glass of water, or two hours after an Ewald test breakfast whether solid contents were still to be found in the stomach,— will serve the practitioner with a simple and ready method which follows naturally in the line of drawing test meals from the stomach, it is however subject to too many physiological variations to permit of accurate deductions. Ewald has proposed the use of salol which according to Nenki is not decomposed by acids (in the stomach), but is converted by the alkaline juices of the duodenum into salicylic acid and phenol. He found in connection with Sievers that the appearance of salicy- luric acid the product of the decomposition of the salol in the urine would indicate that the salol had actually passed out of the stomach. Normally, salicyluric acid will appear in the urine in from 40 to 75 minutes after taking one gramme of salol. Qelay in its appear- ance will indicate a retardation in the passage of food into the in- testines. Salicyluric acid is recognized in the urine by the violet color produced on the addition of neutral ferric chloride solution. You will detect that this method necessitates frequent urination of the patient, every five minutes at least, otherwise the result will not be accurate. Brunner, Riegel and Eichhorst found that the time in which the reaction occured in the healthy individual varied from 40 minutes to two hours. This was to be anticipated as the period that a test meal may remain in the stomach may vary normally between 2 and 3 hours. Plate l Subject and experimenter working at kymograph. LECTURE VIII. METHODS FOR TESTING THE MOTOR FUNCTIONS OF the STOMACH. (Continued.) AS EWALD'S SALOL test is not applicable in private practice P because of the frequent micturition that is necessary, it is im- * possible to examine females, and, also because the excretion of salicyluric acid depends upon the changing energy of the heart's action, intra-arterial pressure, the amount of water in the blood and the changeable function of the kidneys themselves. Huber improved this method somewhat by ascertaining that salicyluric acid disappears from the urine after administration of salol to healthy persons, in 24 hours, but in patients with impaired gastric peristalsis, the reaction continues to be distinct much longer some- times for 48 hours. According to Fleischer and Hecker the duration of excretion of Potassium iodide in the urine of healthy individuals varies from 29 to 55 hours, of sodium salicylate from 21 to 29 hours and in cardiac and nephritic patients this may vary from 80 to 96 hours.—It is evident that methods of such a variable character are not satisfactory for exact research; nor even on account of the great loss of time, of much value for comparative tests. Klemperer's method consists of the introduction of 100 grs. of neutral olive oil into the perfectly clean stomach after lavage, through a stomach tube. Oil or fatty acids which are formed in traces are not absorbed from the stomach. After 2 hours, all oil yet remain- ing is washed out by repeated lavage, dissolved in ether and weighed after removal of the ether by destination. In the normal subject — 52 - Klemperer could find but 20 - 30 grs. of oil, the remaining 70 - 80 grs. had passed into the intestine. If larger amounts are found, for instance 50g, 60g or more, they are according to Klemperer, an evi- dence of motor insufficiency. This method requires very much time and skilled chemical analysis, and, is also open to the same objec- tion as that of Leube. Fleischer (Spez. Path. u. Therap. d. Magen u. Darm. Krankh. page 791.) has proposed a method to determine the gastric peristal- sis by giving 0.1 gr. iodoform in a gelatine capsule during meals; this compound does not decompose in acid media, but does break down in the alkaline juices of the duodenum, and one of its result- ants is potassium iodide which can be tested in saliva by starch pa- per, which, when dipped into the saliva, colors blue on being touched with a drop of fuming nitric acid. Naturally the potassium iodide can also be detected in the urine, but the fact which gives this method the preference over Ewald's salol test is that the KI can be detected in the saliva. It is quite a variable experiment as 1 have discovered; In 23 cases in which I have tried it, the reaction coloring the starch paper first occured just 1 hour after the meal in 12 cases, in 6 cases it oc- cured first in 1 hour and 20 - 22 minutes, in 2 cases in 1 hour and 41 minutes, and, in 1 case in 2 hours;—in 2 cases it took 2Y2 hours to demonstrate KI in the mouth after giving 0.1 iodoform. These were cases in which the gastric secretions were known to be normal. The time of the appearance of the first red and the subsequent blue coloring of the starch paper was carefully noted. Fleischer states that after a test breakfast the reaction in the saliva should occur in from 55 to 105 minutes which is still a considerable margin for variations; too great for practical purposes. Nevertheless the method is interesting and with exactly known meals, might be available for hospital work. In Leube's, Ewald's, Siever's, Klemperer's and Fleischer's meth- ods it will be observed that the gastric motility was determined by something that was administered (salol, iodoform and food.) or poured into the stomach, (oil) and by the absorption of the product of breaking down in the alkaline duodenum and its subsequent ap- pearance in the secretions and excretions, (pot. iod. in the saliva and salicyluric acid in the urine) — an expression in terms of time was Plate II Patient with intragastric bag within stomach and pneumograph in place, both connected with kymograph. — 53 arrived at, to denote the intensity of the gastric peristalsis. In two methods the expression is derived from the quantity of oil or food retained in the stomach after two hours, but also here the result depended upon the passage of something into the duode- num. In all of these methods therefore the fundamental idea is, the rate of expulsion of gastric contents into the duodenum, as if that were the only object of the motor functions of the stomach. It is probable that this, which is only a part of the purpose of the gastric peristalsis, was so much dwelt upon because it offered the most expedient means for experimenting, and, a greater possibility of solution of the problem. However, a second and. most import- ant purpose of the gastric peristalsis, and one, concerning which none of the methods referred to, thus far, can instruct us, is the moving about of the ingesta within the stomach (1) so that they may be made into a more homogeneous mass, (2) so that they may be brought into thorough contact with the gastric juice, and (3) to stimulate the secretion of this juice by the mechanical irritation of the walls of the organ. These in addition to expelling the chyme are the purposes of the motor function. The secretion of the gastric glands is not only stimulated by the mechanical irritation of the stomach walls during peristalsis, but by the contraction of a liberal supply of muscular fi- bers, which arise from the muscularis mucosas, and are spun around the fundus or bases of the gland tubules, the glands are no doubt themselves contracted, and their contents expelled. In some of the batrachians this contraction of the gastric gland tubules by electric stimulation is visible under the microscope. Dr Max Einhorn, the pioneer worker in the pathology and treatment of digestive diseases in this country, has described in the New York Medical Journal Sept. 15 1894 an instrument which re- cords the gastric movements by dots on a narrow piece of paper. This apparatus consists of a ball about yb of an inch (14 milli- metres) in diameter, which is made up of two hollow metallic hem- ispheres which are screwed together. Within this is contained a second smaller ball, which is attached to the upper hemisphere by a non-conductor so that it is insulated from it. The central smaller ball bristles with small metallic spikes ra- diate in all directions, from the center to the inside of the two — 54 hemispheres, but not touching them. A tiny platinum sphere, completes the interior of this apparatus, it lies within the larger round capsule and moves about knocking at the spikes. When it does so, it completes an electric circuit be- tween the outer hemispheres, and the spikes of the central ball; — for two insulated wires, one connected with the hollow ball the oth- er with the spiked ball run up in a very fine, thin, rubber'tube and are connected with the two poles of an electric battery. On con- necting the ball with another part of the apparatus, the "ticker," (very much like the instrument used at the stock exchanges for re- porting the variations in stock by telegraph.) — each motion of it will be recorded by lines or dots on the paper. The ball is swallowed and brought into the stomach by the aid of a few swal- lows of water. It must be born in mind that the paper records the motions of the ball only; this does not mean that it records every motion of the gastric peristalsis. In animals upon which I experimented at the biological labor- atory of the Johns Hopkins University, a rubber, stomach shaped bag was fitted exactly to the interior of the animal's stomach, and, connected with a manometer on the Ludwig kymographion. Rec- ords were taken with the animal's abdomen intact and compared .with those with the abdomen opened; so that the gastric peristalsis could be viewed by the experimenter. The physiological peristalsis is essentially the same whether the animal's stomach is normally contained with the abdomen or expos- ed to view. In my experiments the animals were placed in a large metal case with a glass top, underneath the animal holder, about 2 inches of water was contained in the bottom of the case, which was kept at any desired temperature by a number of Bunsen burners beneath the case. Thermometers were suspended from different parts of the case to keep watch on the temperature, for it is most essential that after an animal's abdomen has been opened, it should be kept at a constant temperature by moist steam; this also insures the viscera against becoming too dry. In a similar manner, Ludwig and H. Newell Martin studied the physiology of the mammalian heart;—Schatz conducted his funda- mental investigations on the contractions of the uterus; — Engel- Plate HI The apparatus, not including kymograph. G, intragastric bag distended; F, the oesophageal tube attached to it; H, intragastric bag collapsed in the shape it is intro- duced, A, pressure bottle elevated and filled with water and graduated; B, stopcock; D, lower graduated bottle, empty at first. The bag is distended after it is swallowed by connecting it at K with D; the stopcock B is turned on, and the water then runs from A to D, displacing the air in D and forcing it into the bag. Both bottles being graduated, the ammount of air in O is always known and can be utilized as an indication of the gas- tric capacity. 55 — mann, his pioneer work on the contraction of the involuntary mus- cle fibers of the ureter;— Phliiger and Haidenhain have done similar accurate work on excised organs, the results have been repeatedly confirmed by other competent investigators. These epoch making experimentations are mentioned to assure you that experiments conducted on organs isolated either entirely (Martin - Ludwig - Engelmann) or partially (Schatz - Phliiger) are capable of giving perfectly physiological contractions or peristal- sis which differ in nowise from the perfectly normal ones. It is frequently urged that these experiments on account of the operations and the anaesthesia necessary, do not present perfectly physiological conditions, and that therefore the deductions made thereform are not logical nor represent the true state of normal functioning. It is undeniable that we never get at the absolutely exact nor- mal functioning of an organ, the stomach for instance during an experiment, as ether and chloroform have an inhibiting effect on the gastric peristalsis. But we are enabled to produce unconciousness of the animal after a brief ether narcosis by brain compression, and then the gastric peristalsis continues perfectly normal. The stomach of the rabbit will show normal peristalsis after complete excision and suspension on a hook or clamp in a warm moist chamber. What brought me to the idea of using an intra- gastric thin rubber bag to record the peristalsis after many attempts with a small sperical bag, that did not exactly fill out the entire lu- men of the stomach, was the repeated observation that the small round bag, such as Prof.. Moritz of Munich used, did not record every peristaltic movement that was visible to the eye when the ab- domen was opened. We frequently noticed peristaltic constrictious of the autrum pyloricum when the rubber bag, of about 12 inches in diameter was at the cardia or fundus, and recorded no movement but that due to the pressure caused by the descent of the diaphragm. We concluded after 3 months experimentation that a small intra-gastric apparatus could not possibly record every peristaltic movement. Sometimes one could witness very strong tonic contractions of seemingly every muscle fiber of the stomach;- it gave that impres- sion, — by which the whole organ contracted from all sides by - 56 shortening of every circular, oblique and longitudinal fiber, and at the same time the bag gave no record of movement, although when it was lying in the fundus it was clearly being lifted up- it would not record until it was compressed by food or the opposite gastric wall. For these reasons, a bag was devised which had the exact shape of the stomach, but could readily be swallowed and when distended within the organ, exactly adapted itself to its interior filling every nook and corner in it. If a little food was needed in the organ we simply did not blow the bag up as far as to fill it out completely. Our apparatus, as has been demonstrated to you many, times on a large variety of cases in the clinical, amphitheater is ajusted with great ease even in patients who are examined the first time. By a pneumograph it records the respiration separately and thus enables one to differentiate the active from the passive movements. A seperate seconds pen gives on the same paper a tecord in time so that the experimenter can at a glance tell the duration be- ginning and end of the peristalsis. Whilst it is the most perfect ap- paratus yet devised for recording the motor function it offers a re- liable means of ascertaining the size and exact capacity, and finally the intra-gastric pressure. No apparatus hitherto devised combines these facilities in such a simple bit of mechanism for taking away the chymograph which should be in every medical school, its im- portant parts are simply the intra-gastric bag and a manometer. In practice a manometer connected with the intra-gastric bag- will answer, with watch in hand the experimenter is able to count the peristaltic movements as they are conveyed to the colum of water. Dr. Einhorn in his new book "Diseases of the Stomach page 96" has gathered the impression that the apparatus is of difficult adjust- ment because in my first report (1. c.) I stated that only such pa- tients are taken as have become accustomed to the stomach tube as the nausea and vomiting first attending the initial introduction of the tube make an exact record impossible, I lay great stress here on the word exact, no intra-gastric instrument, not even Einhorn elec- trode can be introduced the first time without some nausea whilst this may not lead to emesis, it nevertheless has a great influence on the number of gastric movements as all cases we have tried generally show more contractions in the first experiment than in any Plate IV - V PULSE WAVES FROM GASTRIC BAG SHOWING EFFECT OF ABDOMINAL AORTA ON THE STOMACH (WHEN BREATH IS HELD) PART OF A GRAPHIC HISTORY OF DIGESTION OF 100 GRAMMES BEEF 200 ■' MILK 100 " WHEAT BREAD '^aA/- HOLD BREATH HOLD BREATr STOMAUn WAVE STIMULATING PE Curve of contraction of stomach of terrapin, in which slow stimulations- number of stimulations can be so increased pen PRIMARY COIL SECONDS T—r EFFECT OF FARADAIC STIMULATION * CENTIMETRE8 .^i/AAA^ n„. / \rT\°L^ imPUlSe' SS Sh°Wn in the gaStric necord' is not a genuine <*rdiac inhibition, but only a one, due to the fact that the stomach draws away from the diaphragm and aorta during violent contractions and does , TZU™? ' SC "tl P mg thiS Peri°d WaS undisturbed ^d regular. Distance of secondary coil from primal centimetres on the sliding apparatus. GASTRIC PERISTALSIS WHILE BREATH WAS HELD1 ACTIVE (GENUINE) GASTRIC MOVEMENTS S^ «*>■ A AOV° ^9.^^ ^ i"i.................iiiiiiii.........i .....iiiiiii................mini Th of Terrapin) May 16,1895 tie., twenty per second—are more effective than rapid stimulation. The second that the muscle will not contract at all. rfvhf/''W RESPlRATO.l (PASSIVE MOVEMENTS) MOST MARKED IN CARDIAC END n apparent not recieve ry coil, four PNEUMOGRAPH (RESPIRATORY) TRACING Hemmeter's triple intragastric bag. Kymographic record of pyloric (No. i.) middle por- tion (No. ?,) and caodiac end of stomach (No. 3,) in successive peristalsis. — 57 — other. If the record is to be exact and free from objections that may be urged on account of the influence of nervousness, nausea, suggestion, etc., a certain adaptation and experience of the patient is indispensable, no matter what instrument is used. None of these apparatuses will probably be regularly used in practice, they are implements for the trained specialists who know how to apply them and how to interpret their results. Nevertheless you have seen our intragastric bags used regularly at the Maryland General Hospital and good results obtained thereby, even at the first experiment. My objections to the Einhorn gastrograph are that (1) no differentiation between active and passive movements is possible thereby, (2) that there is no coincident record of time in seconds on the paper, (3) that the tonicity or intensity of a contraction can not be adequately determined, (4) that the slow but very extensive general tonic contractions, a narrowing down as it were of the entire stomach to one point in the centre, will probably be recorded by a single dot such as would be made by an inspiration also. At the same time, when we reflect that a bag 12 inches .in diameter may miss some of the contractions and fail to record them, it is difficult to imagine, that the gastrograph should record them all being not even an inch in diameter. Nevertheless Dr. Einhorn's apparatus marks an epoch in the history of stomach motions and their physiology, it is the first at- tempt and largely a successful one to obtain their record by mechan- ical means. It seems of very easy application and when combined with an exact time record it permits of results that for practical pur- poses are sufficiently accurate. Passive motions caused by the pulsations of the aorta and the impulse of the heart ventricles against that part of the saccuscoecus cardiae which touches the arch of the diaphragm, and also the respiratory passive motions due mostly to the muscles of respiration are to a small extent participants in the causes of gastric movements, but they can not of themselves produce evacuations of the contents as we had occasion to observe in the clinic on the hysterical girl. R. H. who had no active stomach movements, no genuine peristal- sis at all, all of her gastric movements were due to respiration and circulation. This girl showed normal state of the secretions after an Ewald - 58 - test meal, but at the same time there was stagnation and over reten- tion of food. It is therefore most essential to be able to distin- guish between active and passive movements, for a person may have a great many movements of the stomach and yet have no genuine peristalsis at all. LECTURE IX. MOTOR FUNCTIONS OF the STOMACH. ONE OF THE intra-gastric, rubber, stomach shaped bags which are used in our clinic, consists of three separated compart- ments; one filling out the pylorus, the second filling out the middle portion of the stomach—the fundus, the third occupying a small part of the fundus and the saccus coecus cardiae. (See New York Med. Journal, Sat, June 22, 1895, page 772.) Each one of these compartments wrote its record on the kymograph by a sepa- rate tambour. In that article I made the assertion from the results obtained with this bag that in the human being most if not all the peristaltic waves start at the pyloric end. This statement was made before Moritz's investigations in the Zeitschrift fiir Biologie were publish- ed, proving that the cardiac end and the fundus of the stomach could not contract, even when stimulated by powerful faradic currents on both, the mucous as well as peritoneal surface. One week before my results were published in the New York Medical Journal, Dr. S. J. Meltzner of New York, published his re- sults with direct and indirect faradization of the digestive canal, which demonstrated quite conculsively that the mucous membrane of the digestive canal offers a considerable resistance to the penetra- tion of the faradic current to the muscular coat, the greatest resis- Intragastric tissue rubber bag, with three distinct parts and three separate outlets for recording the origin and direction of gas- tric peristalsis. Outside of the mouth the triple tube separates in- to its three component tubes, each being connected with a separate tambour and glass ink pen, writing the gastric contractions and relaxations on the kymograph. Part of bag No. i records the con- tractions of the pylorus; portion of No. 2, the middle of stomach, and part No. 3, of the cardiac end. — 59 — tance being found in the mucous membrane of the stomach. The percutaneous and the direct faradization of the stomach or intestines, can not produce any contraction in these parts. Meltzer stated explicitely the kind of instruments used, the sliding inductorium (Schlitten apparat) of Du Bois Reymond — a Groves cell prepared anew for each experiment, and also stated the distance in every case of the primary from the secondary coil. His device of indluding the sciatic nerve of an animal (nerve muscle preparation of hind leg of frog most likely) in the circuit is most ingenious and practical. There is however a very important matter which physiologists must insist on knowing, and which Dr. Meltzer does not state, per- haps because it was not very readily found out, and that is the num- ber of stimulations to the second used by him. Involuntary muscle fibers are much slower to contract than voluntary muscles, and in electrical stimulation experiments, they contract much more readily when the number of stimulations does not exceed 240 per minute. The vibrator on the Du Bois Reymond inductorium was found after months of experimentation to send too many stimulations in- to the stomach per second, when I later on used the Kronecker in- terrupter connection with a Jacquet chronograph and no more than 200-240 stimulations per minute, it was found that the pre antral sphincter could be made to contract with the distance of primary from the secondary coil = O, and both electrodes on the mucosa. To get this result, it is best to make the animal starve for 12 hours, for some reason yet unknown, the contractions are more un- likely to occur, the closer the experiment is made after the ingestion of food. Still it must be emphasized that practically the mucosa of the stomach is a nonconductor. I had occasion to try this in the physiological laboratory recently with a bit of healthy human stom- ach mucosa, that a member of this class tore off from the wall of his stomach during experimental lavage, the piece was 15 m. m. long, 5 -6 m. m. broad, and 2-4 m. m. thick. The gentleman in question, after trying to wash his stomach out and not succeeding to his satisfaction, connected the end of the tube with a suction ap- paratus (aspirator). This was followed by copious haematemesis for which I was hastily summoned. In the stomach tube, partly projecting from the — 60 — lower opening.was a bit of fleshy substance which on microscopic examination proved to be gastric mucosa. After the hemorrhage ceased the young man was treated as if he had gastric ulcer for 1 week. He did not experience any pain during the accident nor thereafter, the only thing that frightened him was the blood. He made a good recovery. This bit of mucosa was placed in a contin- uous circuit with a milliampere meter; the instrument showed 20 milliamperes with circuit uninterrupted, with the bit of gastric mu- cosa in the circuit it showed but j milliamperes. As it was impos- sible to get this fresh piece of mucosa into the circut perfectly dry it is probable that the indication of 3 milliamperes was brought a- bout through the couducting agency of the moisture on the outside of the tissue. In the biological laboratory of the Johns Hopkins University, I have frequently had persons stomach's connected with the kymo- graph, and an intra-gastric rubber bag blown up to fill out their stomachs exactly. Through the intra-gastric bag ran two insolated wires, one ending in a small brass knob near the pylorus, the other coming out against the mucosa in a similar knob near the cardia. Every active and passive motion was recorded by a manometer pen. (N. Y. Med. Jour. June 22. '95 page 771.) But the strongest faradic currants (distance of primary from secondary coil = O) could produce no contractions of the stomach. Dr. Geo. P. Dreyer and myself held one of the poles in our right hand, the plus for instance whilst the negative was in the stom- ach, with the left hand we touched the back of the persons neck, the current was so strong that it became intolerable to us, although this current made its circuit through the patient, it caused no con- traction as evidenced by the manometer in connection with the intra-gastric bag. Frequently we could observe contractions of any skeletal mus- cle upon which the outer electrode was placed—for instance the gas- trocnemius and still the stomach did not contract, this proves that in some conditions the gastric musosa may transmit a current yet the muscular layer give no evidence of contractions. I do not wish to imply that it is absolutely impossible to contract the human stom- ach by electrical stimulation, but the current required to effect this must be so strong that the experiment becomes hazardous. — 61 — Einhorn (Diseases of the Stomach, p. 78-83.) and Paul Cohn- heim (Archivf. Verdanungskrankheiten, Bd. I Seite 274.) have de- scribed tiny bits of mucosa which are found in the wash water and vomit of many gastric sufferers. I can' confirm this observation and add that I have found these pieces of gastric mucosa on washing out the stomachs of perfectly healthy persons. Now it has occured to me that rare instances in which a good contraction of the stomach was obtained, it was due to the fact that the current found its way to the muscular layer, through spots from which the glandular layer had been cast off. It must not be omit- ted to add that all stomachs experimented upon by my method in this series were washed out prior to the experiment to insure absence of current interrupting food particles in the organ. Prof. Moritz of the University of Munich experimented with an apparatus very similar to mine, except that his rubber intragas- tric bag was round, not stomach shaped, it did not therefore exactly and completely fill out the organ, nor did he use the graduated press- ure bottles by which it is possible to determine just exactly how much air is blown into the bag. Instead of a pneumograph, he used a cork in one nostril of the patient which was connected with a second manometer writing on the Ludwig kymograph; the advantage of the pneumograph over this method must be apparent to every one. My first results appeared in print, three months before those of Moritz in the Zeitschrift fiir Biologie Bd. XXXII. Prof. Moritz has made the most important contributions to the physiology of the mo- tor function since the investigations of Hofmeister and Schiitz (Archiv f. exper. Pathol, und Pharfn. 1886 Bd. XX.) In order that you may better understand the mechanism of the gastric peristalsis it is well to bear in mind the arrangement of the muscular layers, (1) longitudinal, (2) oblique and (3) circular, and what was said under the head of anatomy of the gastric layers and the formation of the sphincter of the pylorus. The stomach end near the pyloric part is spoken of more specifically as the antrum pylori. The line of separation between the antrum pylori, and the body or fundus of the stomach, is made by a special thickening of the circular fibers forming what is spoken of as the transverse band by older writers, for instance Beaumont in his Physiology of Digestion 2nd. edit. 1847 page 104 — (a pioneer piece of work, very funda- — 62 — mental and thorough in its observations, this book remains a mon- ument to American Physiological Investigation). Recent observers describe this transverse band as the sphincter antri pylorici and lo- cate it at a distance of 7 — 10 centimetres from the pylorus. In the antrum pylori, as you remember there is a very strong musculature and its glands contain only (or rather mostly) chief, central or ferment cells. The exact character of the gastric move- ments during digestion have been first carefully studied on the hu- man being by Beaumont, his facts and errors have influenced phy- siologists more or less np to the present time. One can not fail to suspect that the stomach of Alexis St. Martin was too far from a normal one, to draw absolutely correct conclusions from. The ex- tensive adhesions which Beaumont describes, certainly acted at times as irritants at others as impediments to normal peristalsis. Prof. W. H. Howell's views on the gastric movements as ex- pressed in his new American Text Book of Physiology, page 317, will serve as an expression of a modern specialist in this branch. He says (I.e.) the movements occur in two phrases: first, the feeble peristaltic movement running over the fundus chiefly on the side of the great curvature, and resulting in pushing the fundic contents in- to the antrum; secondly, the sharp contraction of the sphincter antri pylorici followed by a similar contraction of the entire musculature of the antrum, both circular and longitudinal, the effect of which is to squeeze some of the contents into the duodenum. It is possible that either of these phases, with especially the first, might occur at times without the other, and in the first phase it is possible that the longitudinal fibers of the stomach also contract, shortening the organ in its long diameter and aiding the propulsive movement, but actual observation of this factor has not been suc- cessfully made. It can well be understood that a series of these movements occuring in short intervals would result in putting the entire semi-liquid contents of the stomach into constant circulation. The precise direction of the current set up is not agreed upon, while it is probable that the graphic discription given by Beaumont is substantially accurate. A portion of this description may be quot- ed as follows: The ordinary course and direction of the revolutions of food are, first after passing the oesophageal ring, from right to left, along the small arch; thence, through the large curvature from -63 - left to right. The bolus, as it enters the cardia, turns to the left, passes the aperture, descends into the splenic extremity, and follows the great curvature into the pyloric end; it then returns in the course of the small curvature. The average time taken for one of these complete revolutions, according to observations made by Beaumont seems to vary from 1 to 3 minutes. It is possible, ,of course, that this typical circuit taken by food may often be varied more or less by different conditions, but the muscular movements observed from the outside would seem to be adapted to keeping up a general revolution of the kind discribed. The general result upon the food may be easily imagined. It becomes thoroughly mixed with the gastric juice and any liquid which may have been swallowed, and is gradually disintegrated, disolved, and more, or less completely digested, so far as the proteid and albumin- oid constituents are concerned. The mixing actions are aided, moreover, by the movements of the diaphragm in respiration, since at each descent it presses upon the stomach. The powerful muscular contractions of the antrum, serve also to triturate the softened solid' particles, and finally the whole mass is reduced to a liquid or semi-liquid condition in which it is known as chyme, and in this condition the rhythmic contrac- tion of the muscles of the antrum eject it into the duodenum. The rhythmic spirting of the contents of the stomach into the duodenum, has been noticed by a number of observers through duo- denal fistulas in dogs, established just beyond the pylorus. It has been shown also that when the food is entirely liquid — water for example — the stomach is emptied in a surprisingly short time, within twenty or thirty minutes; if however, the water is taken with solid food, then naturally the time it will remain in the stomach may be much lengthened. Brinton [Diseases of the stomach] advanced the view which dif- fers from Beaumont's in assuming a central current of the food, moving from the pylorus to the cardia through the central long axis in the stomach. There are according to this author two currents, one along each curvature running from the cardia to the pylorus, meeting and turning inward toward the centre of the stomach in front of the pylorus and then running back toward the oesophagus as a single - 64 - central current, there dividing to make again a current as before along each curvature. According to Poensgen, (Die Motor: Verricht: des Menschl: Magens-Strassburg 82.) Reymond, Donders and Lesshaft approved of this theory, — whilst Penzoldt and Foster accept the great food circle of Beaumont. Although I have made over 50 experiments on dogs, cats and rabbits to observe a food circulation within the stomach correspond- ing to these views, and although I have had an opportunity of see- ing into the human stomach, through a fistula during digestion — I have not been able to confirm by actual observation either Beau- mont's or Brinton's views. Whilst I have no new explanations to offer, it has occured to me that the piston like, backward and for- ward movements of the food caused by the antral contractions, and especially of the sphincter of the antrum, is a sufficient force to effect the mixture of the chyme with HCL and the ferments, such as is found in it when it leaves through the pylorus. The views of Beaumont and Brinton date from the epoch, when it was considered all important that food must be properly digested and macerated in the stomach, it was not conceivable then that by far the main bulk of digestion is carried on in the intestines. Hence the complicated theories of Beaumont and Brinton of circular move- ments of food owe their origin to the thought that such a movement was necessary to mix the ingesta with the gastric juice. In dogs this is not proven to occur in every instance; In herbivora (horse, cow.) the centre of the food mass in the stomach may be alcaline or neutral in animals killed one hour and a quarter after feeding. In a number of experiments in which the stomachs' of animals on opening the abdomen were found in active motion; I inserted long needles through the gastric walls to determine the direction they would assume under the pressure of the ingesta; according to Beau- mont, the ingesta moving from the saccus coeccus along the greater curvature to the pylorus, should compel the points of the needles to be directed toward the pylorus when run through the greater curvature, and at along the lesser curvature they should point to- ward the cardia. If Brinton's theory were true, the points of the needles at both curvatures should at least during a large period of gastric digestion — 65 — be directed to the pyloric end. If needles are inserted to a distance of Y* mcn along both curvatures during active gastric peristalsis, a great diversity of movements of the outside portions of the needles is observable. They very rarely point the same way along either curvature, and one portion of them may point toward the cardia, whilst another points to the pylorus. Only when the needles are inserted very deep so that they dip into the central or axial stream, one can occasionally observe what appears as concerted action. During active peristalsis, when the preantral sphincter at times contracts so powerfully as almost to obliterate the lumen, those needles inserted into the fundic portion of both the greater and lesser curvature are strongly turned toward the cardia, but simulta- neously those few needles in the antral and pyloric portion are turned toward the duodenum. The same evidence of a central or axial current which indicates the pumping work of the muscular antrum in pushing back solid particles into the fundus, and squeezing liquid and semi-liquid portions into the duodenum, can be obtained by the intragastric electric lamp when introduced during the heigth of gastric digestion. These lamps can be seen through the abdominal wall in dogs whose abdomen has been shaven, when introduced in a dark room, though naturally not quite so distinct as when the abdomen is opened. Once I observed this axial food current at the clinic in a female patient with very thin abdominal parietes, when the Einhorn intra- gastric lamp was introduced one hour after a meal. In animals with abdomen opened, I have been able to see this lamp carried along the entire greater or lesser cnrvature—during active digestion, but the occurence is so rare as to appear accidental. That the retrogressive current which is set up by contractions of the antrum, forcing the too solid food particles back toward the fundus, must inevitably set up some new movements among the remaining food mass in the fundic end is natural, but I doubt whether it ever reaches that systematic circulation described first by Beaumont and Brinton. It should not be overlooked that if the observations of Beau- mont of a complete food circuit were really true and the only move- ments in addition to the duodenal extrusion which the food mass underwent, there must always be a mass of food in the center of the — 66 — stomach which never touches the gastric wall if all the food moves about along the periphery, there must be a central quiet portion. Brinton was aware of this defect in Beaumont's statements and improved upon them by his still more complicated piston move- ments to explain the axial food motions. If the conditions described by these authors exist, they are not well explained by the arrangement of the muscularis of the fundus, which, as far as the work of Meltzer, (I.e.) Moritz (I.e.) and Gold- schmidt (I.e.) show, is very feeble indeed in its contractions, and hardly sufficient to propel food in any direction, yet according to the above theory, much work is ascribed to it, as the preantral spincter is only 7-8 cm. from the pylorus it certainly cannot be made ac- countable for the movements all around the cardia and the saccus coeccus. The musculature of the fundic end has never been observed in peristaltic motions by myself except those that occasionally arising from the antrum travel upward over it. During active peristalsis it is in a condition of tonic contraction which with the intragastric bag in the fundus, I have estimated is equal to 6 - 8 centimeters of water. (Water manometer.) Moritz, in his work on the motor function of the stomach, stu- diously avoids refering to any systematic food circulation within the organ. It seems rational that sufficient churning and mixing is effected by the powerful contractions of the antrum during the gen- eral tonus of the fundus to explain the saturation and softening of the ingesta by gastric juice. The contrasting relation of the fundus and antrum regarding active peristalsis, are evident in the degree of pressure, as observed on a water manometer in connection with my triple intragastric bag. In the fundus, the pressure is on an average equal to 3 - 6 cm. of water. The increase of intragastric pressure due to cardiac action is equal to 1 - 2 cm. (In this is included the pressure due to every new heart impulse and aortic impulse.) The inspiratory increase of pressure is equal to 6 - 12 cm. These are very nearly the figures Prof. Moritz obtained before me, and, I add them here merely in support and confirmatory of his views. The physiology of the motor function has been dwelt upon more extensively than seems necessary in a condensed statement of — 67 - gastric pathology, not only because it is the most important office of the stomach, but because I have become convinced that in a large majority of disorders of secretion and absorption, (not all) an ab- normality in the motor function lies at the foundation. The exaggerated or diminished peristalsis can on careful examination be detected somtimes before the secretory and ab- sorptive anomalies are apparent. The secretory disturbances ob- served after double vagotomy (section of both vagi) are due accord- ing to Contejean to the motor paralysis caused at the same time. (Archiv de Physiologie 5, IV, p. 640.) A similar view is held by H. Borutteau— (Phliigers Archiv, Bd. 65 p. 26.) The relation between motility and secretion and absorption is not at all well understood, the peristaltic movements effecting a chur- ning motion are those mostly concerned in stimulating secretion, when these movements are lost, secretion is generally lost also. The last vestige of peristalsis left, is that by which the stomach is emptied, and it may be present with total absence of secretion. In stomachs with motility much impaired and secretion arrested the ab- sorptive function is greatly reduced-(Atrophic Gastritis Carcinoma.) In temporary arrest of these functions, the secretive and absorptive functions generally return with improved motility. LECTURE X. .ABSORPTION FROM the STOMACH — PENZOLDT'S AND FABER'S, HERSCHEL'S, JULIUS MILLER'S AND HEMMETER'S TESTS FOR GASTRIC RESORPTION. SHE METHOD most commonly employed is that of Penzoldt and Faber, consisting of 3-5 grains of iodide of potassium enclosed in a gelatin capsule, which is administered with 100 c.c. = }Y ounces of water. Iodide of Sodium or Potassium when tak- en internally, will appear and can be tested for in the saliva and urine where it is excreted in about 6Y tol 5 minutes. The test is made generally by wetting starch paper with saliva of the patient every 2 minutes after the KI is taken, and touching the wet spot with fuming Nitric acid. The first appearance of a blue color indicates that the iodide has reached the point of excretion in the saliva, and consequently must have been absorbed. If this reaction occurs later than after 15 minutes, then the rate of absorp- tion is reduced, this according to Zweifel (Resorpt. Verhaltnisse d. Menschl. Magen Deutch. Arch. f. Klin. Med., Leipzig, Bd. XXXIX, p. 349,1886.) occurs in Gastritis, Dilatation and Carcinoma; in gas- tric ulcer, the resorption is said to be normal or nearly so. Most authorities (J. Wolff, Zweifel, Sticker, Quetsch) differ very much on this matter, but agree on the reduced absorption in - 69 — carcinoma. If the iodide is given during a meal the reaction occurs much later. Herschel — (Indigestion London, 1895, p. 115.) estimates the absorptive power by giving two decigrams of powdered rhubarb. This will give a red color in the urine with liquor potassae normal- ly in 15 minutes. My experience with this method is that frequent- ly the urine is so highly colored in digestive patients that the red color must be very decided to be recognized. In addition to which it suffers from the same objection as Penzoldt's and Faber's meth- od. These are; — In the first place BrandPs experiments have shown that sodium iodide is absorbed to a very slight degree or not at all in dilute solutions. Not until its solutions reach a concentration of three per cent or more does its absorption become important. Accordingly all sol- uble inorganic salts are practically not absorbed in the stomach, since it cannot be supposed that they are normally swallowed in solutions so concentrated as three per cent. Brandl.also found that condi- ments, such as mustard, pepper, also alcohol, very much facilitated the absorption of sodium iodide, perhaps these substances act by stimulating the epithelial cells, or by causing a marked hyperaemia of the mucosa. The absorption time does not vary much in the same individ- ual, except, when the stomach is full; in this case it is not only pro- longed, but is very variable in the same individual. This prolonga- tion according to Sidney Martin (Diseases of the Stomach London 1895) is probably due to a considerable dilution of the iodide by the stomach contents, and also to the fact that the salivary glands are not so active some time after a meal as in the fasting condition. One must not overlook the fact in these experiments, that it is not only the absorptive activity of the stomach that is being investiga- ted, but also the excretory activity of the salivary glands. In Zweifel's experiments it is probable from what we know ©f the absorption of water in the stomach through the observations of Tappeiner (iiber Resorption im Magen—Zeitschr. f. Biol.—Miinchen Band XVI ,p. 497, 1881.) and Von Mering (I.e.)—that most of the liquid containing the iodide passes rapidly into the dnodenum. Therefore we may be testing not only gastric absorption and excre- tory activity of salivary glands, but also intestinal absorption. — 70 — Zweifel concludes (I.e.) that in all diseases of the stomach, there is a prolongation of absorption time which is greatest in dilatation and carcinoma and least in chronic gastric catarrh and very slight in ulcer in the later stages, in the early stages of ulcer however he ciaims absorption is also prolonged. It is very evident that no differentiation between catarrh and ulcer is possible according to this method and thereby one of the main purposes of such investigations, that of aiding in the establish- ment of a diagnosis is thwarted. In view to these defects which apply equally well to Herschel's, Penzoldt's and Faber's methods of testing absorption, and are caused mainly by the fact that water is not absorbed from the stomach, and that the varying secretory activity of the salivary glands is a factor influencing absorption time, I have devised a method which is available for experiments on gastric absorption in the physiolo- gical laboratory, and, which I have successfully tried on six male patients and ten healthy students. The manner of testing the urine or saliva was discarded entirely. My method consists in washing out the stomach thoroughly, then, by means of my method of duodenal intubation, the entrance into the duodenum was plugged or closed up by introducing a small, rubber baloon into it and blowing it up just "in front or beyond the pylorus. (This method has been described also by Dr. F. Kuhn in the Munchener Medizin. Wochschr. No. 27, 28 and 29, 1896, but his method is built upon a different principle from mine—the spiral electrode.) After thus mechanically closing the pylorus, a weighed amount of any harmless inorganic salt, sodium chloride, or sodium sulphate dissolved in 100 c.c. of distilled water so as to make a 3 percent solution, is poured into the organ through a tube, this is indispens- able to exclude loss of the salt solution through clinging to the • tongue, mouth and oesophagus, or absorption from these tissues. After a lapse of 10 minutes, the fluid is again drawn out of the stomach by aspiration, or even if necessary, by adding known quan- tities of distilled water until the last washing gives no indication of containing any trace of the salt by a proper chemical test. (In case NaCl sodium chloride or common cooking salt has been used, a weak solution of nitrate of silver AgN03 can be employed to assure - 71 — oneself that this last wash-water contains no more NaCl. The nor- mal HCL is not secreted so rapidly as to cause confusion in the result.) This entire water is now evaporated to dryness and the residue weighed. The difference between the amount of NaCl poured into the stomach—which in a }4 to ^, the cases of hyperacidity and atrophy is present in from y* to Ys of the cases of anacidity. Adoplf Schmidt, ( Virchow's Archiv, Bd. cxliii, S. 478.) asserts that the epithelium of the surface of the stomach is preserved better than the gland cells in inflammatory conditions of the mucosa, this he says is particularly so in chronic gastritis which forms island like foci in stomachs otherwise not much changed. My experience and that of W. D. Booker, is not in accordance with this observation (see pathology of simple acute and chronic gastritis in the clinical portion of this work). Although I preserved the stomachs by injecting them immediately after death (within 2o min.) with alcohol, also with formaline and sublimate so that autodigestion was at once checked, my sections showed generally a more serious destruction of tne sur- face epithelium than of the gland cells. At times both are so much altered that it is impossible to say which is most or least affected. It seems in chronic gastritis that new epithelium will be reformed quite rapidly where the old has been lost or destroyed. In suspected cases of malignant neoplasms fragments of the growth are occasionally found and are of importance in the diagnosis. In carcinoma of the cardia or the oesophagus they are most frequently found in the lower or side opening of the tube as it must pass through or over the growth on its way into the stomach. But even in malignant growths of other parts of the stomach, patient searching in the sediment of the wash water will sometimes reward the clinician by the discovery of tumor fragments. The first wash water in the morning about 500 c.c. shouldbe permitted 112 to settle 12 hours in a conical glass such as is used for the settling of urinary solid constituents, the sediment should be examined under a low power (about 50 diam.) Once I made the diagnosis of carcinoma when no tumor was evident from repeatedly finding involuntary muscle fibres when no meat had been eaten for 3 days after preceeding lavage. It proved to be a broad flat carcinoma of the posterior wall. The accompanying plates and drawings of normal and patho- logical gastric mucosa were executed by myself. The drawing showing a longitudiual section of the secreting gland tubules show- ing beautifully the well preserved cylindrical epithelium of the gastric surface and well differentiated oxyntic and chief cells was made from several sections of a piece of mucosa that was torn loose by the stomach tube, by a medical student who tried to aspirate a meal that had disagreed with him by means of the pump. The tearing off must have occured in an instant as there are no signs of inflam- mation in the sections. The sections were stained in a variety of ways principally in the eosin-haemotoxylin, Golgi and Bismark brown stains. The minute communications of the oxyntic or parietal cells with the central duct are best brought out by the Golgi method. The drawings of fragments found in the wash water of glandu- lar proliferation with glands closely packed and connective tissue diminished and of glandular atrophy, mucoid degeneration, vacuoli- zation and small cell infiltration are all explained by the text accompanying the illustrations. We have seen that histological chan- ges approaching or actually representing pathological states may be going on in perfectly healthy stomachs. Futhermore, the stomachs of diseased patients may on serial sections, show a different patho- logical state at different places of the mucosa. Therefore it must be borne in mind, that although the findings in hyperacidity and ana- cidity appear to be in some relation to the disease; this kind of investigation must not be relied upon as representing in a given fragment the condition of the entire mucosa. It represents the state of the location from whence it sequestrated, that not being accurately known generalizations must be made with caution. LECTURE XV. OCCURENCE OF SECRETIONS IN THE EMPTY STOMACH — STIMULATIONS TO SECRETIONS OF GASTRIC JUICE • — SIGNIFICANCE OF FOAM —*PREPARATION OF GASTRIC CONTENTS — QUANTITATIVE AN- ALYSIS — METHODS — STANDARD OR NORMAL SOLUTIONS — INDICATORS — TITRATION — APPARATUS. OST AUTHORS are of the opinion that no secretion is con- tained in the empty stomach. Schreiber (Arch.f. exper. Pathol. u. Phar., Bd. xxiv, S. 365, also Deutsche med. Wochsehr., 1894 No. 18-21.) however, concludes that a secretion is found also in the empty stomach, that is he denies a continuous secretion or gastro- succorrhoea as a disease sui generis and claims to be able to obtain 60 c.c. of a secretion possessing good digestive power, from a je- june, fasting stomach before any food has been taken. Pick, (Prager med. Wochsehr., 89. N. 18) who obtained similar results believed that the secretion was set up by the stimulation of the sound used. Rosin, (DeutscL.med. Wochsehr., 1888, No. 47,) A. Hoffman, (Berlin, klin. Wochsehr., 1889, No. 12,) and Martius, (Deutsch. med. Wochsehr., 1894, p. 638.) have also obtained a diges- tive secretion from the fasting stomach. *The section on Quantitative Chemical Analysis of Gastric Contents has been written by my associate, Dr. Edward L. Whitney, whose experience as demonstrator of Clinical Pathology has admirably fitted him for the concise and clear account of this department. It gives me pleasure to express my thanks to him for his assistance. fl - 114 — Although there may be found 50-60 c.c. of a secretion capable of digesting, in the empty normal stomachs of perfectly healthy in- dividuals, this does not prove that a continued secretion exists nor- mally. Riegel, (Deutschmed. Wochsehr., 1893, P 735.) Leo (Krank- heiten d. Bauchorgane p. 54) considers this digestive secretion a residuum of the last, previous meal and seems to have shown con- clusively, that such a residuum is constantly present in the stomachs of infants after a night's sleep (See Leo—Berlin Klin. Wochenschr., 1888 No. 49.) For the practical objects of diagnosis he concludes that a secretion of 50-60 c.c. of digestive fluid found in a fasting organ must not be considered pathological. Only when the amount gained reaches 100-300 c.c. it indicates hypersecretion which is often associated with hyperacidity. Reichmann (Berlin Klin. Wodhschr., 1887 s. 12.) Bouveret I.e. Debove and Remond (Les Malidies de I. Estornac)—Riegel and Reichmann do not distinguish sufficiently between socalled continuous secretion of gastric juice with a stomach of normal capacity and normal exit to the duodenum and continuous secretion which appears as a concomitant symptom of Gastrectasia with probable pyloric stenosis. Einhorn, with more accurate differentiation between these states, it will probably be found that the normal stomach in a fasting state, contains very little if any secretion. I have seen a number cases whose stomachs were of natural size and where there was no disturbance but which contained this secretion early in the morning before breakfast. J. Schreiber (Deutsch med. Wochsehr., 1894, No. 53.) has ex- perimented upon two healthy persons and found gastric juice with hydrochloric acid in both, before any food had been taken. The amount of secretion thus obtained varied from 10 to 22 c.c. Martius (Deutschmed. Wochsehr., 1894, 32.) and Huber (Korrespondentz- blattf. Schweitzer Aerzte 1894, No. 19.) confirm Schreibers results. According to Ewald, who sums up the Literature, (In Lubarsch and Ostertags, Ergebnisse d Sptznf.Pathologie, Bd. 3, S. 27.) and gives his own observations in a large number of cases, this problem is represented in the following manner. In many individuals small quantities of a digestive secretion containing free hydrochloric acid can be obtained from the fasting, jejune stomach, Sometimes it is mixed with bile coloring matter and duodenal contents. But he claims that the stimulation to this secretion has been furnished by - 115 - swallowed saliva, (Martius) remnants of food,pharyngeal secretion, etc., and that the state of things lies between a normal and an abnor- mal one, and that there is no diseased condition of the gastric mucosa. In case of typical Gastrosucorrhoea however, there is a much increased irritability of the mucosa giving rise eventually to a pro- fuse secretion, which, when found in empty stomachs, is quantita- tively more considerable than that found in normal jejune stomachs. Huber compares it to a slow, gradual, dying away of the tonus of secretory irritability (Abklingen des Sekretions reizes) that has been set up by the ingesta and seems to linger after they have passed into the duodeuum. In order to obtain gastric secretion a variety of methods have been suggested. By chemical stimulation, according to Leube's method which consists in allowing 50 c.c of a y} solution of sodium bicarbonate flow into the stomach. After 12 minutes this is washed out again and .should be found neutral. By thermic stimulation according to Jarworski's method, consisting of the introduction of 100 c.c. of ice water and washing it out again after ten minutes when it should con- tain acid and pepsin. These methods if successful at all, bring out the gastric juice in a most diluted state and therefore give no ade- quate means to determine the secretion by chemical analysis. It has been claimed by Einhorn (New York med. Record, 9 Nov. 1889) and Allen A. Jones (Ibid 1891) in this country, and, Hoffman (Berlin klin. Wochsehr., 1889, N. 13) Ewald I.e. and Ziemssen, in Germany that the gastric secretion, as evinced by the amount of hydrochloric acid could be increased by faradic or galvanic stimu- lation. Whilst I have my doubts about this matter I do not wish to imply that electricity is not a very valuable therapeutic agent in the treatment of digestive diseases; we could not in fact dispense with it as an auxilliary to treatment. In my opinion the influence of electricity on secretion is not yet satisfactorily proven. As a means to obtain gastric secretion this method is certainly not available. The normal secretions are best obtained by the natural stimulation of one of the test meals given on page S7 and 88. Among the list there mentioned the test meal of Fleiner should have been stated which is similar to Riegel's test dinner and consists of a plate of soup a portion of tender beef steak or roast beef and po- 116 — tatoe puree. Mathieu and Remond [Soeiete de Biolog 1890] have published a method to determine the total quantity of stomach contents by finding out the acidity of the undiluted contents as much as can be drawn then that of the contents as much as can be gained by washing out the stomach with a known quantity of water and from this the acidity of the total amount of contents that were originally in the stomach are calculatd. Strauss (Therapeutisehe Monatshefte Marz 1895), has simplified this procedure, but for the practioner it is sufficient to know the amount gained by the simple methods of drawing the contents by expression or aspiration. Concerning the recognition of proteid and carbohydrate indigestion from the food remnants it should be added this is much facilitated by the double test meal used at our hospitals. In Gastrectasias presence of foam indicates gas fermentation. Gas may be found even in presence of normal or supernormal t amount of hydrochloric acid, since F. Kuhn (Zeitsehr., f. klin. Medi- cin Bd. xxi and Deutsch Med. Wochsehr., 92, No. 49) has demonstra- ted that the hydrochloric acid of gastric juice has no detrimental effect on large amounts of yeast. Whenever there is stagnation of gastric contents this gas formation can occur. After the contents of the stomach are withdrawn, they must be prepared for and submitted to chemical examination. The contents may be beaten up thoroughly to make a homogeneous mixture and the chemical examinations conducted on this mixture, or this mix- ture may be filtered and the clear filtrate subjected to analysis. The former method gives the more accurate results, with slightly higher acidity, than the latter method; which has the advantage however of allowing better observation of color changes in the solution during titration. Before entering upon a discussion of the chemical methods as applied to to the gastric juice, a short description of the methods, solutions and apparatus required in quantitative analysis will be given. The solutions required can be made up, and if preserved from the influence of sight and air, can be kept indefinitely. The methods used in quantitative chemical analysis may be divided into two general classes; Gravimetric and Volumetric. The — 117 — Gravimetric methods consist of the isolation of the substance or one of its compounds which is weighed. The isolation of sub- stances in a pure state often requires long training in chemical me- thods, and if a small amount of the substance in question is present it may be very difficult to separate a weighable amount unless large quantities of the mixture are available. Many substances can not be separated from mixtures without losing at the same time their relation to other substances in the same solution. The great objec- tion to the Gravimetric system however is the large amount of costly apparatus necessary, and the length of time needed for the manipulations. The Volumetric methods are more easily performed, in this, the quantity of the substance under examination is ascertained by a calculation based upon a measured quantity of a solution of a known strength required to perform a certain reaction with it. These solutions called standard solutions, are of two kinds, normal solu- tions and Empirical solutions. A Normal Solution is one which contains in a litre, a quantity of the active reagent, expressed in grammes and chemically equi- valent to one atom of hydrogen. Decinormal Solutions, N10, are one tenth the strength of nor- mal solutions. Centinormal Solutions, N100, are one hundredth the strength of normal solutions. Empirical Solutions are those which do not contain an exact atomic proportion of the reagent, but are made up of such strength that one c.c. is equivalent to some definite weight of the substance sought. Residual titration or back titration consists in treating the sub- stance tinder examination with standard solution in excess of that known to be required, the excess is then ascertained by residual ti- tration with another standard solution. In general, titration results in the formation of a compound that can be distinguished by its properties, from those substances present in either solution. 1. It may form a precipitate. 2. It may cause the complete solution of some precipitate. 3. A slight excess of either reagent, may produce some visible — 118 — change in some constituent of the solution, or a change in some substance added for the purpose. (Indicators.) 4. The indicator in some cases can not be added to the solution but from time to time a few drops of the solution are added to the indicator on the side. Of the above solutions, the normal solution is the most used, the empirical solution being only of limited application. It would seem a simple matter to make up a standard solution which would be perfectly accurate, but the problem is not so simple. Absolutely pure chemicals are not easily obtained, and such as are easily obtained, unmixed with other mineral substances, contain a variable amount of water, and are moreover exposed to more or less danger of contamination from the impurities of the air. The following methods of obtaining a tenth-normal solution are recom- mended as a basis for the preparation of other solutions. 1. Pure, dry, oxalic acid is obtained and the crystals that show no sign of efflorescence selected. From the formula, C2 H2 04+2 H2 O, it is seen that the molecular weight is 126, and as it is a dibasic acid, the normal solution would contain one half of this, (63grammes) dissolved in distilled water and made up to one Litre, at a temperature of 15°C, As a tenth normal, N10, solution is re- quired; one tenth of this or 6.3 grammes are made up to a litre as before and used to correct the solutions used in analysis. It must be noticed that oxalic acid in dilute solution soon decomposes so that it must be freshly prepared as required. To prepare anequivalant solution of caustic soda (decinormal NaOH) about five grammes of caustic soda are dissolved in about 800 c.c.of distilled water and well mixed. To this there is added lime water or baryta water Ca (OH)2 or Ba (OH.)2 as long as a precipitate forms, to get rid of carbonates or sulphates. The solu- tion is allowed to stand until the impurities have settled. Twenty- five c.c. of the solution are then measured with a pipette into a clean flask or beaker and titrated with the above solution of oxalic acid, using a few drops of phenol phthalein as an indicator, until the red color of the solution just disappears. The solution is then diluted to the strength of a decinormal solution. As an illustration of the method of ascertaining the amount of dilution necessary to make the two solutions exactly equivalent, we — 119 — will suppose that the twentyfive c.c. of caustic soda solution requi- red 28.3 c.c. of the oxalic acid solution to discharge the red color. If twentyfive c.c. of the caustic soda solution neutralize 28.3 c.c. of the acid solution, then the amount of caustic soda solution necessary to neutralize 1000 c.c. of the acid solution will be found by the fol- lowing proportion. 28. 3 : 25 : : 1000 : (x) x = 883. 4 x = amount of of caustic soda solution necessary for 1000 N10 NaOH. Dilute 883. 4 c.c. of the caustic soda to 1000 c.c. with distilled water. After diluting the solution it should be again titrated to ensure its accuracy, and if properly standardized it should be changed from red to colorless and vice versa by the addition of a drop or two of the acid or alkaline solutions respectively. The titration should be conducted as rapidly as possible to avoid the error produced by absorption of C02 from the air and all solutions kept in well stop- pered bottles for the same reason. 2. About eight grammes of pure dry sodium carbonate are heat- ed in a platinum crucible for ten minutes at a dull red heat, stir- ring occasionally with a platinum wire. After heating, it is pow- dered in a warm mortar and allowed to cool in a dessicator. When cool, 5. 3 grammes of the powder are weighed rapidly, washed into a flask with hot distilled water and made up to a litre. -This con- stitutes a decinormal solution of sodium carbonate. A decinormal solution of sulphuric acid is prepared in the fol- lowing manner. About three c.c. of the pure strong acid, of a specific gravity of 1. 840, is made up to about 900 cc. This approximate solution is standardized against the sodium carbonate solution prepared as above, using a drop or two of a—0.1$ solution of methyl orange as an indicator. Twenty-five c.c. of the acid solution is titrated with the decinormal sodium carbonate until the red color shown by this indicator in acid solution turns to a light yellow. The correction of the approximate solution is made from a proportion upon exactly the same principle as in the former case (Nol.) To correct this decinormal solution of sulphuric acid for very accurate work, the following method is recommended. One hun- dred cc- of the decinormal solution of sulphuric acid is alkalinized — 120 — with a strong solution of ammonia— (ammonium hydrate.) The solution is evaporated to a constant weight on the water bath and the amount of sulphuric acid calculated from the amount of am- monium sulphate formed. Indicators.— An indicator is a substance used in volumetric analysis which indicates by change of color or some other visible effect, the exact point at which a given reaction is complete. Generally the indicator is added to the substance under exami- nation, but in a few cases it is used, outside, a drop of the substance being brought in contact with a drop of the indicator. The particular uses of the indicators will be more fully ex- plained in their proper places, under the quantitative examination of the gastric juice, but the chief ones in use in such examinations may be briefly mentioned. Tincture of litmus which turns red in acid solution, blue in an alkaline solution. It is used in solution, and also in the form of test-papers. (It is not used when carbonates are present.) Phenolphthalein solution, a 1$ solution of phenolphthalein in alcohol, colorlesss in acid solutions, red in alkaline solutions. Is not reliable for alkaline phosphates, bicarbonates, or ammonia. Methyl orange solution, a 0.1$ solution of methyl orange in water turns red with acids, yellow with alkalies. It is not affected by carbonic acid, and is valuable for titration of alkaline carbo- nates. The other indicators and their uses in analysis of the gastric juice will be mentioned later. Apparatus.— The apparatus needed for volumetric work is comparatively simple. Burettes, measuring flasks, measuring cylinders, and pipettes. An accurate balance is required in all chemical work, delicate to a milligramme and weighing up to say fifty grammes. Burettes, are glass tubes graduated to tenths of a c.c. and holding from 25 to 100 c.c. They are provided at the lower end with a rubber tube and pinchcock by means of which the amount of the solution can be accurately regulated. The tube is graduated upon its outer surface and the amount of the solution used, can be read off from this graduation. The simplest form of burette is the one already described, known as Mohr's, of which various modifications are in use. — 121 — Measuring flasks are vessels made of thin glass, having a narrow neck, and so constructed-that a certain amount of fluid reaches a graduation placed about the middle of the neck. These flasks are of various sizes, 100, 200, 250, 500 and 1000 c.c. Measuring cylinders, are of various sizes, from 25 to 1000 c.c. graduated from. 0.5 to 5 cc. Pipettes are of two kinds, those graduated for one quantity only, and. those graduated on the stem to deliver various quantities. A convenient set for Stomach work is the following 2, 5, 10 and 25 C.C. In addition to the above apparatus, one should be supplied with funnels, crucibles, beakers, flasks, test tubes, Bunsen burners, etc. All apparatus should be kept scrupulously clean, rinsed before and after using with distilled water. It is well to wash the inside of any measuring apparatus two or three times with small portions of the solution for which it is to be used. Greasiness interferes very much with accurate reading. It may be removed by dilute alkaline solution. The burette should be placed perfectly perpendicular, and firmly fastened. Fill by a funnel, the stem resting against the in- ner surface of the burette, to avoid the formation of bubbles. Al- ways fill above the zero-mark, gently tap the burette until the bubbles disappear should they be form. Then run out a small portion (or down to the zero mark) remembering to run out enough to remove all air bubbles from the bottom of the burette. In reading the results, always read from the bottom of the meniscus, formed by the rising of the outer borders of the liquid along the sides of the burette. LECTURE XVI. CHEMICAL EXAMINATION ON GASTRIC JUICE — TESTS FOR PRESENCE OF FREE ACIDS — TESTS for FREE HYDROCHLORIC ACID — THE DIM- ETHYL-AMIDO-AZO-BENZOL TEST — THE KESORCIN TEST — COM- BINED HYDROCHLORIC ACID — LACTIC ACID: FORMATION, SIGNIFICANCE, DETECTION. EACTION: The reaction of the gastric juice, obtained by means of the stomach tube or otherwise, after the admini- stration of a test meal, is always acid in the normal individ- ual. The reaction is best determined by dipping into the juice, a piece of very delicate blue litmus paper. In juice of acid reaction the paper immediately turns red. Very rarely is the reaction alkaline, this being found only in a few cases of atrophy of the gastric mucosa, occasionally in acute gastritis, and when for some reason, a portion of the intestinal contents and the alkaline bile has been forced back through the pylorus in sufficient quantity to neu- tralize the acid of the stomach. In severe cases of gastric atrophy the reaction is usually acid, even in absence of fermentative changes. This is due to the presence of acid salts, such as acid sodium phosphate (Na H2 P04,) and of traces of organic acids, which occur in nearly every test meal in quantities sufficient to produce an acidity of from 6 to 10 degrees. R - 123 - TESTS FOR PRESENCE OF FREE ACIDS. A delicate test for the presence of free acids is found in Congo red. Congo red occurs as a fine reddish brown powder, dissolving readily in water to form a clear deep red solutiom, which changes in the presence of free acids to a dark blue. This substance may be used in two ways as an indicator. 1. A solution is prepared by dissolving one grm. of the powder in 100 cc. of water, and adding a small drop to a few c.c. of the gastric juice. If the juice contains even a slight trace of free hydrochloric acid, or the organic acids in slightly larger quantities the solution immediately turns a bright blue. 2. A test paper may be prepared by soaking bibulous paper in the above solution of the dye for several hours and then care- fully drying. This paper is simply dipped into the filtrate or into the contents before filtration and exhibits the same color reaction as the solution mentioned above, and has the additional advanta- ges, of being more convenient, and, exhibiting as readily slight changes in color. It has been found also, that when the acidity is due to organic acids and not to free hydrochloric acid, the color can be made to disappear by warming gently over the open flame. On the contrary if the acidity is due to hydrochloric acid, the dark blue stain on the paper changes to a lighter tint but does not disap- pear except when strongly heated. It must be emphasized that this color change from red to blue does not occur in solutions of acid salts or in the presence of com- bined hydrochloric acid and therefore indicates the presence of some free acid, inorganic or organic. « TESTS FOR FREE HYDROCHLORIC ACID. Many tests have been proposed for free hydrochloric acid, the following given in the order of their accuracy and delicacy being probably the most reliable. 1. Dimethyl—amido—azo—benzol 0.02 p. m. 2. Phloroglucin—vanillin 0.05 p. m. 3. Resorcin 0.05 p. m. — 124 — THE DIMETHYL— AMIDO—AZO—BENZOL TEST. This test, recently introduced by Topfer, is probally destined to replace all others in the clinical laboratory, both on account of its simplicity and also on account of its ready application tothe direct quantitative estimation of the amount of free hydrochloric acid in the gastric juice. This indicator occurs in the form of a brown powder, readily soluble in alcohol, only slightly soluble in water. A few drops of the alcoholic solution, added to a solution of hydrochloric acid turns a bright cherry red, increasing in intensity as the strength of the acid solution is increased. In the absence of free hydrochloric acid or other mineral acid the solution turns a bright lemon-yellow. In actual practice a 0.5$ solution of the substance in alcohol is employed. A few drops of this solution are added to the stomach contents which need not be filtered for this purpose, or to the resi- due left in the receptacle in which the stomach contents were recei- ved. If free hydrochloric acid is present the cherry red color deve- lops and spreads in beautiful rings from each drop of the indicator, usually leaving in the center a clear yellow area. In case the indi- cation is doubtful the following modification may be employed. A small porcelain evaporating dish (or white butter plate) is throughly rinsed with distilled water and dried. Upon one side of the dish a few drops of the filtrate are placed and upon the opposite side a single drop of the indicator. By inclining the dish gently the two solutions may be made to mix and, at the line of junction, the cherry red color may be seen, the white back ground rendering the detection of the tint less difficult. It has been stated by Einhorn, and others that this test is liable to mislead in cases in which there is a large amount of organic aci- dity. It is true that in the presence of lactic acid amounting to 0.2$. or more in gastric juice this test yields a red color resembling that due to inorganic acids but the objection in more theoretical than real, as the presence of such an amount of organic acids sel- dom occurs in the stomach and in the presence of proteids, peptones mucin etc, still stronger solutions of the organic acids are required to produce the characteristic reaction. Futhermore the quantitative estimationt of organic acidity to be described presently will show the necessity of employing further - 125 — tests for the presence of free hydrochloric acid, on account of a specially great acidity of organic acids, which does not occur in a stomach secreting a normal amount of hydrochloric acid. THE PHLOROGLUCIN VANILLIN TEST. The modification of this test proposed by Boas gives the most satisfactory results. Two grammes of phloroglucin and one gramme of vanillin are dissolved in 100 grammes of 80$ alcohol. The solution must be kept in a dark colored, well stoppered bottle as the solution soon decomposes when exposed to the light. The original Giinzberg formula was composed of the same amount of the ingredients dissolved in 30 cc. of absolute alcohol. This solu- tion still more readily undergoes decomposition and has no advan- tages over the above modification. The solution is employed in the following manner; four or five drops of the reagent are mixed on a small porcelain dish, or small butter plate with an equal amount of the filtered gastric juice or the unfiltered gastric contents. This is placed on a water bath, kept just below the boiling point, and evaporated slowly. If free hydrochloric acid be present in the propor- tion of 0.5 p. m. or more a fine rose tint will develop at the edge of the drop where the mixture is dried. The mixture may be evaporated over a naked flame with the same results provided the temperature is not raised above the boi- ling point. If too much heat is applied, a brown or brownish red color may develop, which resembles the color produced where free hydrochloric acid is absent. The rose color produced by this rea- gent only comes from free mineral acids; organic acids, acid salts, combined hydrochloric acid, peptone and albumose produce only a brown or yellowish discoloration. THE RESORCIN TEST. The solution consists of five grms. of resorcin [resublimed] and three grms. of cane sugar dissolved in 100 c.c. of 94$ alcohol. Six drops of the filtered gastric juice and three drops of the solution are mixed on a porcelain plate and slowly evaporated as in the phloroglucin-vanillin [Giinzberg] test. Care must be employed that too much heat is not applied, as heating too strongly simply yields a brown or black deposit. If the operations be properly conducted and free hydrochloric acid be present a fine vermilion — 126 — red line forms at the edge of the drops, following down the edge of the solution as evaporation proceeds, while the color at the pe- riphery gradually fades, disappearing entirely after a short time, lea- ving a reddish brown stain. This test has the same degree of de- licacy as the phloroglucin-vanillin test and the advantage of much greater stability, retaining its delicacy for months while the latter lasts only a few weeks. Many other tests might be mentioned some of them much less delicate, among them tropaeolin OO Mohr's reagent, methyl violet, and emerald green, but the three described will be found the most reliable and easily applied. COMBINED HYDROCHLORIC ACID. If albuminous bodies are treated with a weak solution of hy- drochloric acid it is found that a certain amount of the hydrochloric acid combines with the albuminous bodies to form compounds which do not give the reactions of free hydrochloric acid. In other words certain affinities of the albuminous substance must be satura- ted before hydrochloric acid appears in the free state. In the stom- ach the same reaction must take place except probably to a grea- ter extent due to the more complicated chemical processes through which these substances pass. This is shown by the fact that even after a simple test meal a certain amount of time elapses before the presence of free hydrochloric acid can be demonstrated. In the Ewald meal from 30 to 40 minutes elapses before free hydrochloric acid can be demonstrated in the normal individual while in the more complex meals, considerably more time is required. This form of hydrochloric acid is important in as much as it constitutes a part of the physiological hydrochloric acid and stomach digestion will proceed in a fairly normal manner if enough hydrochloric acid is secreted to saturate these affinities while not enough is secreted to form the excess or reserve supply called free hydrochloric acid. It is evident therefore that if free hydrochloric acid is present all these affinities must be saturated, while in the absence of free hydrochlo- ric acid, some hydrochloric acid, enough to more or less saturate these affinities may have been secreted. The entire absence of hydrochloric acid both free and combined if more than temporary, is a serious condition, indicating an atrophy of the gastric mucosa — 127 — or a severe gastric catarrh. From these considerations it will be seen how important the determination of the combined hydrochlo- ric acid is, in all conditions of anacidity. The estimation and quan- titative determination of the combined hydrochloric acid will be de- ferred to the paragraphs devoted to the quantitative determination of hydrochloric acid. The following table* shows the amount of pure hydrochloric acid necessary to combine with 100 grammes (or 100 c.c.) of the various food stuffs. Milk................................... Sweetbread (boiled).... Calve's brain (boiled) Liver sausage................ Mettwurst........................ Blood sausage................ Graham bread.............. Pumpernickel................ Wheat bread.__............. Rye bread........................ Beer (German).............. Beef (boiled).................. Mutton (boiled)............ Veal (boiled).................. Pork (boiled).................. Ham (raw)...................... Ham (boiled).........._....... Cervelat sausage.......... Swiss cheese.................. Fromage de Brie.......... Edam cheese.............__ Roquefort cheese.......... LACTIC ACID; FORMATION, SIGNIFICANCE, DETECTION. It was formerly supposed that lactic acid was secreted by the stomach, but by the more accurate investigations of later years, it has been shown beyond doubt that lactic acid in the gastric con- tents is either introduced as such in the food or is the pro- duct of abnormal fermentative changes in the food after ingestion. Lactic acid may be introduced in food either as sarcolactic acid 0.32 to 0.42 gramme of pure HCL. .............. 0.9 0.G5 .............. 0.8 ..._.......... 1.0 ().:-5 " .............. 0.3 .______ 0.7 .._'.......... 0.3 ............... 0.5 ..0.07 to 0.13 li - .............. 2.0 grammes .............. 1.9 ............... 2.2 .............. 1.6 ............. 1.9 .............. 1.8 _____ 1.1 .............. 2.0 .............. 1.3 .............. 1.4 2.1 *Erlich:—Dissert Erlangen, 1893. - 128 — from meat or fermentation lactic acid found in bread and other starchy foods. Lactic acid may be formed after the food is ingested, in cases of carcinoma of the stomach, and probably also in small amounts in other conditions, of subacidity or anacidity associated with deficient motility. In the great majority of cases of carcinoma of the stomach lactic acid is present in considerable amounts, except in those cases in which the motility is not impaired. In such cases only a small , amount of lactic acid can be demonstrated usually and in some ca- ses its presence can not be demonstrated. There are cases of carci- noma of the fundus or body of the stomach in which the motility is so good that at the end of one hour, no remains of the test meal can be regained. Small traces of lactic acid can usually be detected for some time after the adminestration of the Ewald breakfast or similar meals, though at the height of digestion tne usual tests are negative, due either to the absorption of the lactic acid or the interference of free hydrochloric acid or of the products of digestion with the delicacy of the tests. In cases in which it is desirable to prove the formation of lactic acid within the stomach, it is necessary to employ some meal which is entirely free from lactic acid. Such a meal has been proposed by Boas consisting of oatmeal gruel to which only a little salt has been added. The stomach is washed out on the evening preceding the administration of the meal until no food particales can be found, the gruel given in the morning and the contents removed one hour after. Only rarely, under such conditions, is any notable amount of lactic acid to be demonstrated except in cases of carcinoma of the stomach. The easiest clinical test for the presence of lactic acid is that of Uffelman. Ten c.c. of a 4$ solution of carbolic acid are mixed with twenty c.c. of water, and a drop of a strong solution of ferric chloride added. A beautiful amethyst blue color is produced which turns a canary yellow when treated with a solution of lactic acid or gastric juice containing lactic acid. The delicacy of this test is interfered with by the presence of free hydrochloric acid and by presence of peptones. Glucose, acid phosphates and alcohol give a reaction resembling that of lactic acid, butyric acid* giving a much lighter tint. In case of doubt, a modification that has given good 129 - results is the following: Five or ten c.c. of the filtered gastric juice are treated with ten times its volume of ether free from alcohol and then shaken in a stoppered separating funnel for fifteen or twenty minutes and allowed to stand till the layers have separated. The ethereal solution is allowed to evaporate, the residue dissolved in five or ten c.c of water, and the solution tested for lactic acid in the same manner. While this test is not a very delicate one, lactic acid when present in considerable amounts gives a more decided reaction than any of the substances mentioned as having a similar reaction, and is a good test for clinical purposes. Boa,s' method is to be employed in doubtful cases. This method is based upon the fact that when lactic acid is treated with strong oxidizing agents, foimic acid and acetic aldehyde are formed. C,H603 = CH3COH + HCOOH. Acetic aldehyde may be easily recognized by its action on Nessler's reagent, or upon an alkaline solution of iodine in iodide of potassium. Nessler's reagent is prepared in the following man- ner. One hundred c.c. of a 4$ solution of iodide of potassium is warmed and while warm treated with iodide of mercury until a small amount remains undissolved. After cooling forty c.c of wa- ter are added. Two parts of this solution are then treated with three parts of a strong solution of caustic potash, any precipitate which may form is filtered off and the reagent kept in a well stoppered bottle. The solution of iodine is prepared by mixing a solution of io- dine in iodide of potassium with caustic potash or potassium carbo- nate. Method: The filtered gastric juice is tested for the presence of free acids as above, and if present ten or twenty c.c. are treated with an excess of barium carbonate. If no free acids are present this is not necessary. The solution is now evaporated to a syrup on the water bath to drive off the fatty acids. The syrup is treated with a few drops of phosphoric acid and brought to a boiling point to expel carbon dioxide. After cooling it is extracted with one hundred c.c. of ether by shaking for half an hour. After standing for a short time to allow separation to take place, the ethereal layer is drawn off and evaporated [avoiding a flame] the residue taken — 130 — up in forty-live c.c, of water, shaken and filtered. The filtrate is treated in an Erlenmeyer flask with five c.c. of strong sulphuric acid and as much black oxide of manganese as will lie on the point of a knife blade. The flask is closed with a perforated stopper, in which is placed a bent glass tube, the long arm passing into a cylinder filled with ten or fifteen c.c. of the Nessler's reagent or al- kaline iodine solution prepared as described. Carefully heat the flask and if lactic acid is present, aldehyde will distill over forming- aldehyde mercury, yellowish red in color, if Nessler's reagent is used and yellowish crystals of iodoform, which may be recognized by their odor, if the alkaline solution of iodine is employed. . 1. Butyric acid can usually be determined by its odor alone which is that of rancid butter. In case of doubt, ten c.c of the gas- tric juice are extracted with fifty c.c. of ether, the ethereal solution evaporated, the residue taken up with water. The odor is more evident in this concentrated aqueous solution. A small amount of calcicum chloride causes the separation of an oily layer of butyric acid, strong mineral acids also separate the oily layer or drops of the acid. Acetic acid may also be detected by its odor. 2. Ten c.c. of the gastric juice are extracted with ether, the ether evaporated, the residue taken up with a small amount of wa- ter, accurately neutralized with caustic soda solution and mixed with a few drops of a very dilute solution of ferric chloride. In the presence of acetic acid this gives a dark red color. 3. The ethereal residue after evaporation is taken up with a small amount of strong sulphuric acid and alcohol. If acetic acid is present the fragrant odor of ethyl acetate is easily detected. Fatty acids do not occur normally in the stomach contents Butyric acid may be formed when a large amount of milk or car- bohydrates have been ingested, usually associated with an excess of lactic. It has been show.n also that butyric acid can be formed from lactic acid. Acetic acid on the contrary is a product of alcohol and may be formed from alcohol ingested or from alcohol produced by the ac- tion of yeast upon the sugar contained in the stomach contents. Hence it follows that it is necessary to exclude alcoholism before sig- nificance is attached to the presence of acetic acid in the stomach - 131 contents. If in the case of acetic acid, alcoholism be excluded, and in the case of butyric acid the ingestion of butter or fats in general be excluded, the presence of these acids has the same significance as the occurence of lactic acid viz, stenosis of the pylorus with dil- atation and fermentation. LECTURE XVII. QUANTITATIVE ANALYSIS OF THE STOMACH ACIDS. KjUMEROUS methods have been devised for the estimation of the JI amount of free hydrochloric acid, present in the gastric juice. ' The most convenient method of estimation for clinical purposes is that of Ttfpfer, which at the same time, estimates the acidity due to organic acids and acid salts, and that due to the combined hydro- chloric acid. Method: Three indicators are used in this method; 1. A 0.5$ alcoholic solution of dimethyl-amido-azo-benzol. 2. A 1.$ aqueous solution of alizarin. 3. A 1$ alcoholic solution of phenol phthalin. 1. As has been mentioned under the head of tests for free hy- drochloric acid, dimethyl—amido—azo—benzol reacts to very faint traces of mineral acids particularly hydrochloric, reacts to organic acids only when present in very large amounts, and not at all to combined hydrochloric acid or acid salts. It will be seen that by this indicator we can easily find the amount of free hydrochloric acid. - 132 - Ten c.c. of the filtered gastric juice are measured into a small clean flask and a few drops of dimethyl—amido—azo—benzol ad- ded. The solution turns a bright red in the presence of free hydro- chloric acid. The solution is now titrated with a decinormal solu- tion of caustic soda, (prepared as above) until the red color of the solution changes to a clear yellow. 2. Into a second beaker or flask, ten c.c. of the gastric juice are measured, a few drops of the alizarine solution added and' the solution titrated with the decinormal solution of caustic soda until the solution turns to a clear violet color. As this tint is difficult for the unpracticed eye to recognize, Topfer recommends the following preliminary tests. (a) To five c.c. of distilled water, add two or three drops of the alizarine solution. A clear yellow color results. (b) To five c.c. of a one per cent solution of disodiuum phos- phate add the same amount of the alizarine solution. A reddish color with a slight tinge of violet results. (c) Five c.c. of a one per cent solution of sodium carbonate when treated with the same amount of alizarine give a clear violet tint, which is the tint to be reached in the titration. Until the eye becomes accustomed to the reaction it is well to prepare this solu- tion as a guide in the titration. 3. To a third portion (ten c.c.) of the filtered gastric juice, two or three drops of phenol-phthalein solution are added and the solution titrated with the decinormal solution of caustic soda. After a certain amount of the solution, has been added, a light rose color develops, which is not however the end of the reaction. It will be noticed that as the drop of caustic soda solution falls into the so- lution, a dark red color is produced at the place of contact, fading into rose color on agitation. The titration must be carried on un- til the entire solution has reached this color and no line of sepa- ration can be made out on adding a drop of the caustic soda solu- tion. There are two ways of stating the result of the titrations: The simplest method is to state the number of c.c of the caustic soda solution which would be necessary to neutralize one hundred c.c. of the gastric juice as that number of degrees of acidity. For exam- ple the number of c.c. of the caustic soda solution necessary to neti- - 133 - tralize ten c.c. of the gastric juice, using dimethyl—amido—azo— benzol as an indicator, is 2.3 c.c. One hundred c.c. would then require ten times that, the amount of acidity being stated as twenty- three degrees. The second method of stating the results is to give the amount of acid per mille in terms of hydrochloric acid. As each c.c of the solution of caustic soda will neutralize O.OO365 gramme of pure hydrochloric acid, the above example would show O.8395 gramme of hydrochloric acid per mille or O8365 per cent. As an example of the calculations employed in Topfer's method, let us suppose that in the titration (1) with dimethyl—amido—azo benzol as an indicator, 3.5 c.c. of caustic soda solution were em- ployed, (2) with alizarine 4.9 c.c. of the caustic soda solution were required and (3) with phenol phthalein 7.5 cc. of caustic soda so- lution were required to produce the proper tint, using in each case ten c.c. of the stomach contents. 1. As dimethyl—amido—azo=benzol reacts only with free hydrochloric acid, the acidity referable to this is 35 degrees or .12775 per cent. 2. Alizarine shows the tint of an alkaline reaction when the free hydrochloric acid, organic acids and acid salts have been neu- tralized, combined hydrochloric acid having no effect upon it. Hence it follows that by subtracting the amount of free hydrochloric acid from the acidity found by alizarine, the amount of acidity due to organic acids and acid salts will be found, in this case 49—35=14 degrees or .0511 per cent. 3. Phenol phthalein only turns to a dark red color when all the acidities of the solution have been saturated, including the com- bined hydrochloric acid. The amount of combined hydrochloric acid may be found by subtracting the acidity found by alizarine from that found by phenol pthaleine, in this case 75—49=26 degrees or .0949 per cent. Method of Martius and Luttke:— By this method, the amount of physiological hydrochloric acidr the free and combined hydrochloric acid are found as well as the total chlorine of the gas- tric juice by determination of the amount of chlorine. The method is based upon the fact, that by' moderate incineration, the free hy- drochloric acid can be driven off, while the chlorine in combination — 134 — with the inorganic bases is not affected. For this method the following solutions are required: 1. A decinormal solution of hydrochloric acid which can be prepared by standardizing against the decinormal caustic soda solu- tion as described in a former chapter. 2. A decinormal solution of nitrate of silver, containing 25$ of pure nitric acid. This solution is approxinately made up by dis- solving 17 grammes of pure crystallized nitrate of silver in 900 cc of a 25$ solution of nitric acid and adding 50 c.c. of the liquor ferri sulphur oxydati of the German pharmacopoeia (the liquor ferri oxysulphatis N.F.) will serve the same purpose. The solution is then standardized against the solution of hydrochloric acid and diluted to the proper volume. Each c.c of the solution is equiva- lent to O.OO365 gramme of pure hydrochloric acid. 3. A decinormal solution of ammoniun sulphocyanate. Eight grammes of the pure salt are dissolved in 900 c.c. of distilled water and titrated against the decinormal solution of silver nitrate. After ascertaining the strength of this solution it is diluted so that it is exactly equivalent to the decinormal solution of nitrate of silver. Method:—1. To determine the total amount of chlorine present in the gastric juice, fence of the stomach contents after thorough mixing, are measured into a small cylinder graduated to 100 cc. and treated with twenty c.c. of the solution of nitrate of silver. The mixture is thoroughly shaken and allowed to stand for ten minutes. The mixture is then diluted to 100 cc. once more agitated, and filtered through a dry filter into a dry flask. Fifty cc. of the fil- trate are then titrated with the decinormal solution of ammonium sulphocyanate until a permanent red color appears. Multiply the number of c.c. of ammonium sulphocyanate by two as only half the filtrate was taken and subtract from the number of c.c. of nit- rate of silver added, (20) the result will be the number of c.c. of the nitrate of silver solution precipitated by the total chlorine of the gas- tric juice and correspond to the same number of c.c. of decinormal so- lution of hydrochloric acid, the whole amount of chlorine being ex- pressed in terms of hydrochloric acid. 2. To determine the amount of chlorine in combination with inorganic bases. Ten c.c. of the filtered gastric juice or of the well mixed sto- 135 - mach contents are evaporated to dryness in a platinum or porcelain crucible over a water bath or on a plate of asbestos to avoid loss from sputtering. The incineration is carried only to the point when the residue ceases to burn with a luminous flame. After cooling the residue is treated with distilled water up to about 100 c.c. or until the filtrate comes away free from chlorides- which may be shown by treating a drop of silver nitrate. If the filtrate re- mains perfectly clear after the addition of a drop of nitrate of silver the residue is free from chlorides. To the clear filtrate is now added ten c.c. of the decinormal solution of nitrate of silver and the excess titrated by means of the decinormal solution of ammonium sulphocyanate as before. The amount of ammonium sulphocyanate solution subtracted from the amount of the silver solution (ten c.c) gives the amount of silver precipitated by the chlorides remaining after incineration, in combination with the inorganic bases. By subtracting the result of the second process from that of the first, the amount of free hydrochloric acid and of combined hydrochloric acid is determined. Modifications:— 1. By titrating with decinormal caustic so- da solution using dimethyl—amido—azo—benzol as an indicator we obtain the amount of free hydrochloric acid, this subtracted from the combined amount of free and combined hydrochloric acid, will give the amount of combined hydrochloric acid. 2. By determining the total acidity with phenol phthalein and subtracting from it the amount of free and combined hydro- chloric acid we can estimate the acidity due to organic acids and acid salts. ). The amount of organic acid present may be estimated in terms of hydrochloric acid by the method of Hehner—Seeman (to be described later.) This result deducted from the result of the preceding (No.2.) test gives the amount of acidity due to acid salts. Leo's method: Leo bases his method upon the fact that when calcium carbonate is added in a fine powder to the gastric juice, the free and combined hydrochloric acid combine with the calcium car- bonate to form calcium chloride, a neutral salt, while the acid salts are not affected. During the reaction however the calcium chloride reacts with the phosphates to form acid calcium phosphate, (mono- calcium phosphate, CaHPO,.) As this requires double the amount — 136 - of caustic soda solution to neutralize that would be required for the acid sodium phosphate, it is necessary to add each time an excess of calcium chloride solution before titration. Method: Ten c.c. of the gastric juice are shaken up with fifty c.c of ether to remove organic acids. The residue after drawing off the etheral layer is treated with five c.c. of a concentrated solution of calcium chloride and titrated with the decinormal solution of caustic soda using phenol phthalein as an indicator. This deter- mines the acidity due to free and combined hydrochloric acid and to acid salts. A second portion of fifteen c.c. is treated with a small amount of pure dry calcium carbonate the mixture stirred and immediately filtered through a dry filter. The carbon dioxide is expelled from the filtrate by passing a current of air through it. Ten c.c. of the filtrate are then treated with five c.c. of the saturated solution of calcium chloride and titrated as above. The acidity found is due to the acid phosphates. By subtracting the result found in the second titration from that of the first, the amount of free and combined hydrochloric acid is determined. Boas' Method: This method is an easily applied test for free hydrochloric acid which gives fairly accurate results in the absence of organic acids or when they are present only in traces. Ten c.c. of the filtered gastric juice are titrated with decinormal caustic soda solution until a small amount (a drop) removed 'by a glass rod, fails to change the tint of congo paper. Instead of using the paper as an indicator outside, a small bit of the congo paper may be dropped into the solution and the titration conducted slowly, with constant shaking until the paper regains its original red color. This test however can not be employed in the presence of any consider- able amount of free organic acids. LACTIC ACID — QUANTITATIVE ESTIMATION. A simple clinical test for lactic acid has been devised by Strauss. A separating funnel is graduated to five cc. below and twentyfive c.c. above. The funnel is filled to the five cc. mark with gastric juice and ether added to the twenty-five cc. mark. The funnel is corked and well shaken and after standing for a short time to allow the fluids to separate, the liquids are run out to the five c.c. mark. Distilled water is added to the twenty-five c.c. mark - 137 - and the mixture treated with two drops of a solution of the offi- cinal tincture of the chloride of iron diluted 1:10. On shaking the mixture, an intense green color is produced if lactic is present in the proportion of 1 p. m. or more. If present in the proportion of from 0.5 to 1 p. m. only a pale green color is produced. Boas' Method: This method of estimating the amount of lactic acid depends upon the oxidation of lactic acid into aldehyde and the estimation of aldehyde by means of a standard solution of iodine. Solutions Required: 1. A decinormal solution of iodine is prepared by dissolving twenty-five grammes of potassium iodide in about two hundred c c. of water, and dissolving in this 12.6 grammes of resublimed iodine. The solution is diluted with distilled water to 1000 cc. and requires no correction. 2. A decinormal solution of sodium arsenite. Dissolve 16.5 grammes of sodium arsenite in about 900 cc, of distilled water. It is then titrated against the decinormal solution of iodine and dilu- ted so that the two solutions are equivalent. 3. Hydrochloric acid (Sp.Gr. 1018.) 4- Normal solution of potassium hydrate (56 grammes in 1000 c.c.) 'Method: Ten or twenty c.c of the filtered gastric juice are tested for the presence of free acid, if present a small amount of barium carbonate is added, if free acid is absent this addition unnecessary, and evapo- rated to a syrup. A few drops of phosphoric acid are added and the solution boiled slightly to expel carbon dioxide. Allow the syrup to cool, extract with 100 c.c. of ether free from alcohol, after the two fluids have separated draw off the ethereal so- lution, evaporate, take up "the residue in 45 c.c. of water, filter. The filtrate is treated in an Erlenmeyer flask with five c.c. of sulphuric acid and a small amount of manganese dioxide. The flask is closed by a two holed rubber stopper, one aperture being closed by a glass tube and rubber tubing clamped off, the other opening receiving a bent glass tube leading to the distilling apparatus. The distillate is received in a large flask well stoppered. The mixture is distilled at a gentle heat until about four fifths of the fluid has passed over. - 138 - The distillate is then treated with twenty c. c. of the decinormal so- lution of iodine and the same amount of twenty cc. the normal potassium hydrate solution, thorougly shaken and allowed to stand for a few minutes in the flask. Twenty c.c. of hydrochloric acid and an excess of sodium bicarbonate in powder are then added and the excess of iodine determined by titration with the solution of sodium arsenite. The sodium arsenite is added until the solu- tion is decolorized, fresh starch solution added and the iodine solu- tion added until the blue color becomes permanent. Each c.c. of the iodine solution in excess of the sodium arsenite solution is equivalent to O.OO3388 gramme of lactic acid. Fatty Acids: The Method of Cahn and Mehring modified by McNaught is simple and fairly accurate. The total acidity is determined in ten c.c. of the filtered gastric juice by titrating with a de- cinormal solution of caustic soda using phenol phthalein as an in- dicator. Ten c.c. are evaporated to a syrup on the water bath, made up to the original volume with distilled water and the acidity determined as before. The difierence in acidity will be the amount due to fatty acids. Total Organic Acids: The total organic acids are best estimated by the method of Hehner—Seeman, called by Leube, Braiins method. Ten c.c. of the gastric juice are accurately neutralized with a decinormal solution of caustic soda using phenol phthalein as an indicator. This solution is then evaporated to dryness, carefully avoiding sputtering, and incinerated as long as the residue burns with a luminous flame. After cooling, the residue is extracted with boiling distilled water, filtered, and the amount of sodium carbonate formed determined by titration with a decinormal solution of hy- drochloric acid. As the presence of free carbon dioxide interferes somewhat with the delicacy of the reaction when phenol phthalein is used as an indicator, the following modification has given better results. After the incinerated mass has been extracted with boiling water and filtered, a known excess of the decinormal solution of hydrochloric acid is added, the solution boiled to expel any carbon dioxide in solution, and the excess of acid determined by back tit- ration with a decinormal solution of caustic soda. - 139 — This method is based upon the fact that when salts of the organic acids with the alkalies are incinerated at a low heat, the carbonates of the alkalies are formed with the liberation of water and carbon dioxide. LECTURE XVIII. DIGESTIVE FERMENTS — PRODUCTS OF DIGESTION — TESTS FOR SAME. SALIVA. The saliva as found in the mouth is the mixed secre- tions of all the salivary glands. It may be readily obtained for testing by requesting the individual under examination to chew a piece of soft rubber or other insoluble substance to stimu- late the secretion and as it forms it is placed in a clean receptacle. It is a clear, slightly opalescent fluid, of a slimy consistency, having a specific gravity of 1002 to 1006. Under normal conditions it has a slight alkaline reaction, its alkalinity averaging in man 0.08 per cent expressed as sodium carbonate (Chittenden.) Its active constituent, ptyalin, acts most readily upon boiled starch, raw starch being protected from its action by the coating of cellulose surrounding each granule. Its action is entirely amyloly- tic, as it has no action upon other food products. Its action upon starch may be demonstrated in the following simple manner. A few c.c. of boiled starch paste are treated in a test-tube with a few drops of saliva. A few drops removed and treated on a testing plate with a few_drops of iodine solution give — 140 — the characteristic blue color of starch. After a moment or two a few drops removed will show a violet color, and by treating a por- tion at intervals the color changes gradually to a deep reddish brown and finally disappears. Different products of the action of the ferment are found at different stages of digestion. The violet color first found is a color which results from a mixture of erythrodex- trin and starch when treated with iodine. Later the color becomes reddish brown due to the change of the starch entirely into dextrins and sugar. When digestion has gone on until the solution gives no color whatever with iodine, the solution still contains some form of dextrin (achroodextrin) as may be shown by the addition of alco- hol which throws down a profuse white precipitate. It may be shown also that the solution contains sugar by treating a small amount of the mixture with Fehling's solution. This sugar according to the investigations of Nasse, v. Mering and Musculus is not dextrose as formerly taught but maltose. The action of ptyalin is most energetic at the temperature of the body. It acts best in a neutral medium though a small trace of alkali has little or no effect upon it. Its activity is stimulated by the addition of enough acid to combine with its proteid consti- tuents. A minute trace of acid still allows the action to continue, but for practical purposes we may say that the addition of free acids in such quantity as are found in the gastric juice, not only stop its action but entirely destroy the ferment so that after neutralization, it is no longer able to digest starch. In the stomach the action of the ptyalin probably continues until the presence of free acid destroys the ferment. As no free acid can be demonstrated in the gastric until the laspe of fifteen or twenty minutes normally, the greater portion of the starch is trans- formed into sugar and acho6dextrin. Under normal conditions then we should find in the gastric juice removed for examination, sugar, achroodextrin, and a faint trace of erythrodextrin. The pres- ence of a marked reaction of erythrodextrin then is valuable pre- sumptive evidence of hyperacidity, its absence indicating either nor- mal, acidity or subacidity. Only in rare cases have cases of the absence of ptyalin from the saliva been seen. There are some unexplained cases in which with a normal or — 141 - diminished acidity, even the digestion of starches is very poor, as is shown by the marked reaction of erythrodextrin and the small per- centage of sugar found by quantitative test. The activity of the salivary excretion ought always to be examined in such cases. Pespin. The proteolytjc ferment of the gastric juice is active only in an acid medium and is destroyed by very dilute solutions of the alka- li carbonates. Pepsin is probably not secreted as such, its precurs or being pepsinogen or propepsin which is transformed by weak acids into the active ferment, pepsin. While hydrochloric acid acts best in thus transforming pepsinogen into pepsin, other acids to a lesser degree perform the office. Pepsin, like the other ferments has the property of changing an almost unlimited amount of pro- teids providing the products of its action are removed when for- med, and the temperature kept at a favorable point, as it appears to act by its presence, not being itself destroyed or changed by the reaction. While no quantitative methods have been devised, and it has never been isolated in a pure state we know that a product can be obtained by complex chemical methods, which, while intentsely proteolytic, exhibits none of the reactions of exproteids, so that the ferment whatever its nature probably is not a proteid. The only tests which can be used for its detection therefore are of a quantitative nature, its effect in acid solution on proteid sub- stances. Comparative tests may also be instituted, using for com- parison, gastric juice from a healthy stomach. The amount of acid necessary for the most vigorous action of •pepsin varies with the form of proteids employed. For example, pepsin acts best on fibrin when the acidity is about one per thou- sand, while coagulated egg albumen is digested most rapidly when the acidity amounts to two or three per thousand of hydrochloric acid. Test. Three test tubes or small wine glasses are taken and a small thin slice of boiled egg albumen placed in each. To the first is ad- ded three c.c. of the gastric juice; to the second, three c.c. of the gastric juice to which hydrochloric acid has been added in sufficient quantity to bring the acidity to two or three per thousand; the — 142 — third is acidulated as in number two and a few grains of pepsin ad- ded. The three tubes or glasses are now placed in the warm oven at a temperature of 40°C and allowed to remain for three hours. If at the end of this time all three tubes show digestion by the rounding off and solution of the egg albumen the specimen con- tained pepsin, if number two and three only, show digestion the contents contained pepsinogen but no pepsin, while if only the third tube or glass shows traces of digeston the specimen contained neither pepsin nor pepsinogen. Pepsinogen. This substance is supposed to be excreted by the cells of the gastric mucosa, and to be changed into pepsin by the action of the hydrochloric acid of the gastric juice. This action has been differ- ently explained by various experimenters, the most plausible theory being that a combination of the two takes place, with the formation of pepsin hydrochloric acid. In the absence of hydrochloric acid, this body, pepsinogen, may be present in normal amount and require only the addition of a sufficient quantity of hydrochloric acid to bring the gastric juice to a normal acidity, to render the stomach contents active. In the absence of free-hydrochloric acid, we may test for the presence of this substance by acidulating with hydrochloric acid as in number two of the pepsin test, adding a small bit of boiled egg albumen and placing in an oven at a temperature "of 40°C. for three hours, at the end of this time noting the presence or absence of signs of digestion. Boas employs a comparative test which in doubtful cases may yield valuable information. Properly labeled tubes are prepared, and in them are placed measured quantities of gastric juice diluted with a solution of hydrochloric acid of the normal strength of the gastric juice (two or three p. m.) so that the tubes contain the gas- tric juice in dilutions of 1 : 10, 1 : 20. To each tube a small flake of egg white or fibrin is added and put in a warm oven at the tem- perature of the body. From the amount of dilution at which diges- tion ceases an idea may be gained of the amount of pepsin or pep- sinogen which any gastric juice contains. For comparison, similar tubes may be prepared of normal gastric juice, and the digestive power of the two compared. - 143 - Rennet and Rennet Zymogen. In addition to pepsin the gastric juice also contains a ferment or its zymogen, whose special property appears to be the precipita- tion of casein from milk. As in the transformation of pepsinogen into pepsin, hydrochloric acid is required, so rennet zymogen, in the gastric juice, is not transformed into rennet except in the presence of hydrochloric acid. Certain neutral salts of lime, such as calcium chloride have however the power of transforming rennet zymogen into rennet even in neutral or slightly alkaline solution. The following tests for the presence of rennet and its zymogen have been devised by Boas. Rennet. Five c c of the gastric juice are exactly neutralized with a de- cinormal solution of caustic soda, five c.c. of neutral milk added, and the mixture after being well shaken is placed in an incubator at the body temperature. If rennet is present the casein will form a firm coagulum in from ten to fifteen minutes. A relative quantitative estimation of the rennet ferment may be performed by the following method: The gastric juice is accurately neutralized and portions of this diluted with distilled water, in known proportions 1 : 10, 1 : 20 etc. To five c.c. of each of these dilutions, five cc. of neutral milk are added and the tubes placed in the thermostat at the body tempera- ture for fifteen minutes. At the end of this time the tubes are re- moved and the dilution at which no coagulation takes place is no- ted. In stating the dilution note must be taken of the fluid ad- ded in neutralizing. Rennet Zymogen. Five cc. of the gastric juice are rendered faintly alkaline by the addition of a decinormal solution of caustic soda, one c. c. of a one percent solution of calcium chloride and five c.c. of neutral milk are added. The tube is placed in the thermostat and after fifteen minutes should show a firm cake of casein. Quantitative. The gastric juice is rendered faintly alkaline by adding a deci- normal solution of caustic soda and dilutions prepared, 1 : 10,1 : 20 etc., estimating in the dilution the amount of fluid added in alka- — 144 — linizing. Five cc of each of these dilutions are placed in test tubes with five c.c. of neutral milk and one cc. of a one per cent solution of calcium chloride. These are placed in a thermostat at the body temperature and at the expiration of fifteen minutes the dilution at which the enzeyme fails to act is noted. From the observations of Boas and others it appears that the secretion of the ferments and the proenzymes is less affected by the minor disturbances which may cause a temporary arrest of the acid secretion of the stomach. De- crease in the activity of the ferments on the other hand usually is the result of some organic change in the gastric mucosa. By experiment upon normal individuals it has been found that rennet is active in dilutions of from 1:30 to 1:40 and rennet zy- mogen in dilutions varying from 1:100 to 1:150. It has been found that even in the absence of free hydrochloric acid the ferments may be active up to the limit observed in normal individuals and that in such cases the condition of anacidity was a temporary mat- ter, due to some mental or circulatory disturbance, the acid reap- pearing when the cause of the disturbance was removed. On the other hand, in cases of anacidity in which the rennet zymogen was active only in the stronger dilutions 1 : 5,1 : 10 etc., the anacidity is due to some organic change in the gastric mucosa from which recovery is usually rare. It will be seen from these considerations, of what importance the quantitative investigation of the gastric ferments is from the prognostic standpoint. Action of Pepsin on Proteids. The action of pepsin upon proteids as has been shown, only takes place in an acid medium. The action is a very complex one and is not as yet fully understood. The first result seen of the action of an hydrochloric acid solution of pepsin upon a coagulated albu- men such as egg-white is apparently a partially mechanical change. The egg white swells up, its edges become rounder and it becomes clearer and more glassy in appearence. The egg white then be- gins to dissolve as is shown by the presence in the solution of a substance precipitated by neutralization which may be called syn- tonin or acid albumen. This action takes place also in acid solu- tions to which the pepsin has been added. The next step is one in which the pepsin plays an important part. The syntonin or acid — 145 — albumen is changed first into the primary albumoses protO-and hetero-albumose. These undergo further change and become deu- tero albumoses and finally peptones. These substances may be distinguished from each other by the following reactions. Native albumens may be removed from the solution if present by rendering the stomach contents faintly acid if not already so and boiling. The precipitate will consist of the native proteids, viz, al- bumen and globulin. (b) The solution is carefully neutralized by the addition of a weak caustic soda solution. The precipitate will consist of syntonin or acid albumen. The neutralization must be exact as the precipi- tate is dissolved by an excess of acid or alkali to form acid albumen or alkali albumen respectively. (c) The filtrate from which the albumen and acid albumen has been removed is now saturated with magnesium sulphate and filtered. The precipitate which consists of the primary albumoses, proto and hetero albumose, is dissolved in water, placed in a dialy- ses and the salts removed by dialysis. As hetero-albumose is in- soluble in pure water it is precipitated by the removal of the salts as in a dialyser. The proto-albumose remains in solution as it is soluble in water and may be tested for by acidulating with nitric acid in the cold, the precipitate redissolving on heating. (d) Deutero albumose or secondary albumose is detected in the following manner; A sufficient quantity of the gastric juice is freed from albumen and acid albumen according to (a) and (b). The filtrate is saturated with powdered ammonium sulphate and the precipitate which forms, consisting both of primary and secondary albumoses is filtered off and the precipitate washed thoroughly with a saturated solution of ammonium sulphate. The precipitate is redissolved in the least amount of water possible, faintly acidulated with acetic acid and saturated with com- mon salt which precipitates the primary albumoses, leaving the deutero-albumose or secondary albumose in solution. After filtra- tion the secondary albumose may be detected by saturating again with ammonium sulphate; any precipitate which may form consisting ofdeutero-albumose. It may be detected also by adding a considerable amount of common salt to its solution and acidulating with nitric acid. A precipitate will form in the presence of deutero-albumose — 146 — redissolved on heating. (e) Peptone may be detected by precipitating all the other pro- teids by saturating with ammonium sulphate and filtering. The filtrate contains the peptone which may be tested for by the biuret reaction. The filtrate is treated with an excess of caustic alkali and few drops of a very dilute solution of copper sulphate. If peptones are present in the solution, a pink or rose red color appears. PAET SECOND. The Gastric Clinic. ACUTE GASTRITIS. Simple Acute Gastritis, Phlegmonous or Purulent Gastritis, Suppurative Inflammation of the Gastric Mucosa, Abcess of the Stomach, Infectious Gas- tritis, Gastritis Mycotica or Parasitasia, Gastritis Diphtherica and Crouposa, Toxic Gastritis, Gas- tritis Venenata. CHRONIC GASTRITIS. GASTRIC ULCER. GASTRIC CARCINOMA. ULCUS CARCINOMATOSUM. MOTOR INSUFFICIENCY OR DILATATION. GASTROPTOSIS. ACUTE GASTRITIS. 1. Simple Acute Gastritis. 2. Phlegmonous or Purulent Gastritis—Suppurative Inflammation of the Gastric Mucosa — Abscess of the Stomach. 3. Infectious Gastritis — Gastritis Mycotica or Parasitasia — Gastritis Diphtherica and Crouposa. 4. Toxic Gastritis — Gastritis Venenata. QASTRITIS is a collective or generic term which comprehends all inflammatory processes proper of the stomach, including the so-called catarrh of the superficial layer of columnar epi- thelium, the inflammation of the glandular parenchyma and inter- stitial connective tissue, the purulent infiltration of the submucosa and, muscularis, and also the penetrating excoriations of corrosive poisons. It is natural that these manifold morbid conditions should pre- sent considerable variations in etiology as well as in the intensity of the symptoms. It is almost impossible to draw a sharp limit separating the simple superficial catarrhs from the deeper, penetra- ting inflammations. Penzoldt suggests the line between mucosa and submucosa. We may designate, as simple Gastritis that inflammation of the gastric mucosa which involves not only the superficial colum- nar epithelium, but as a rule the glandular parenchyma. This con- — 2 — dition may occur in an acute and in a chronic form and under each classification the acute and the chronic gastritis, one may arrange two subdivisions; (1) the primary and (2) the secondary gastritis. We therefore have (1) the acute simple primary gastritis which occurs as the original disease, and (2) the acute secondary gastritis known as the gastritis sympathica acuta which occurs not as the original disease, but as a frequent accompaniment of numerous acute febrile disorders. All the exanthematous infectious diseases, measles, scarlatina, variola, typhus and typhoid fevers, puerperal fe- ver, pyaemia dissentery, croup and diphtheria are known to effect pathological changes in the gastric mucosa directly or to influence it detrimentally by reflex nervous action (Hoppe Seyler Allgemeine Biologie, 1877, p. 242.) There is a very plausible desire evident in some recent works on the subject to avoid the name Stomach or gastric catarrh, because the word catarrh has reference to a superficial inflammation but in gastritis we are dealing also with parenchymatous inflammation Penzoldt uses the expression simple gastritis for an inflammation reaching no deeper than the submucosa (Gastritis simplex) for the penetrating results of suppurative or purulent inflammation, he uses the term (Gastritis gravis) Grave gastritis. He does not favor the terms toxic and infective gastritis for to a certain extent all forms of this disease are toxic and infective and in his book (Specielle Therapie Innerer Krankheiten, Vol. iv, p. 320) he dicusses only (1) simple and grave acute, secondly (2) chronic gastritis and thirdly [3] purulent or suppurative gastritis. Fleischer (Specielle Therap. u.Pathol, d. Magen u. Darmkr. S. 79}- ) describes (1) simple acute, (2) secondary or sympathic acute, [3] phlegmouons or puru- lent [4] toxic [5] diptheritic, croupous, mycotic, parasitic [6] chronic gastritis. Excepting those forms mentioned by Fleischer under group 5, Boas describes all of these in separate chapters. Ewald mentions and describes all of these forms and subdi- vides the suppurative inflammation [the Gastritis phlegmonosa puru- lento] into an idiopathic primary and a metastatic secondary form. Sidney Martin's treatise of the organic and functional diseases of the stomach deals with the symptomatology, pathology and treatment of acute and chronic gastritis in one chapter [the viii] and then goes on it to speak of toxic and infective gastritis in the next chap- - 3 - ter [the ix]. Albert Mathieu of Paris, briefly mentions acute and chronic gastritis and the varying amount of mucus and acid accom- panying these diseases, none of the other forms are referred to [ Wm. Wood Edition, X. Y.] Rosenheim, [Pathol, u. Therap. d. Krankh. des Verdauungs ap- parates, p. 99] describes gastritis acute, simple, phlegmonous, toxic, diphtheritic and chronic. Einhorn approaches the simple classifi- cation of Penzoldt and divides acute gastritis into [1] simple, [2] phlegmonous and [3] toxic and then proceeds to the consideration of chronic gastritis. Alois Pick describes [1] acute, [2] infectious, [3] phlegmonous, (4) toxic, (5) parasytic and (6) chronic, (Vorlesungen iiber Magen u. Darmkrankheiten, S. 73-) and Fleiner (Lehrbuch d. Krankheiten d. Verdauungs organe) gives an account of (1) gastritis catarrhalis acuta for which he also uses the name Gastricismus, [2] Gastritis toxica, [3] Interstitial suppurative gastritis, stomach abscess and stomach phlegmone, or gastritis phlegmonosa, or interstitialis, or submucosa purulenta, or also Linitis suppurativa, [4j Mycotic gastric inflam- mations, (5) Chronic gastritis. Osier, in his new principles and practice of Medicine p. 348- 359, consider; — Acute simple, (2) phlegmonous or acute suppura- tive, (3) toxic, (4) Diphtheritic or membranous, (5) Mycotic or par- asitic, (6) chronic gastritis, under the latter he gives a special para- graph to the chronic forms with extreme connective tissue prolifer- ation, increase in thickness of the submucosa and muscularis under the name of sclerotic gastritis. These references are sufficient to demonstrate the discrepancy existing in latter works concerning the separate and distinct recog- nition of the various forms of this disease and that a more uniform classification would be desirable. In accordance with Penzoldt, this treatise will describe only (1) simple acute gastritis, (2) simple chronic gastritis and separately, (3) the forms in which the element of pus formation is a factor, the suppurative gastric inflammations and in a supplement the forms due to toxic or corrosive agents and the remaining very rare varie- ties may be appropriately described. One should be very careful not to diagnose every temporary, transient gastric disturbance as acute gastritis, nor a prolonged loss — 4 — of appetite, with eructations, coated tongue and no other demon- strable signs and symptoms as chronic gastritis, as Penzoldt correctly says this is in the majority of- such cases, neither justifiable nor conductive to scientific development of diagnosis. We can agree with im in the opinion that it is inconceivable that all the func- tional and anatohiical changes, which, one is accustomed to find in acute inflammations in other tissues, should really be present in every brief digestive disturbance after dietetic errors, alcholic abuse, etc. We could not designate a brief irritation of the nose with sneez- ing secretion of mucus and hoarseness, lasting several hours, as nasal catarrh. By catarrh of the air passages we understand a more lasting affection with a somewhat typical course and more perma- nent changes in the mucosa of both a structural and functional na- ture. Indeed Sidney Martin very appropriately considers these functional, lighter forms of gastric disturbance under a separate chapter and classifies them under (1) gastric irritation, (2) gastric in- sufficiency. Functional disorders, then are irregularities of gastric motility, absorption and secretion, and also of the innervation and vascular supply, in which organic disease of the organ-ulcer, gastri- tis, neoplasm, etc., are absent. It can not with certainty be stated that all histological changes are absent in functional disorders, at least in functional disorders of secretion. I have become convinced of certain changes in the acid and ferment cells that are apparently quite constant. - Ever since Beaumont's pioneer observations it has been known that every severe inflammatory irritation of the gastric mucosa produces an alteration in the gastric secretion, the quantity and effectiveness of which is much reduced; it is known futhermore that the impairment of one function of the stomach as a rule, rapid- ly involves that of another. The inner lining of the stomach can not in its true anatomical meaning of the word be called a mucus membrane, because it is devoid of one of the essential attributes of a mucus membrane, the mucus glands. The mucus of a normal stomach is surprisingly small in amount and owes its origin not to glands but to mucoid degeneration of the superficial columnar epithelial cells. As this cylindrical epithelium continues down into to the al- - 5 — veoli of the peptic tubules without any distinct border line, all irri- tants striking the former must of nesessity affect the parietal or border cells as well as the chief cells of the gland duct. It is charac- teristic for the pathology of gastric digestion, that impairment of one important function or rather of one of of the many physiolo- gical processes of which the digestive act is composed, soon creates sympathetic disturbance in the remaining functions so that the clin- ical picture of an acute or chronic gastritis is that of a combination of disturbances. It is not established nor very essential, which function suffers first, but probably in most cases a derangement of secretion starts the morbid series and the remaining functions follow in the affec- tion; For example, if by ingestion of food which is already in a state of fermentation an acute gastritis has been induced, the reduc- tion in the amount of hydrochloric acid produces a hindrance not only in the normal chemistry of the stomach but resorption and mo- tility are also very soon retarded. This pronounced subacidity has in its consequence an imperfect digestion of the proteids so that very small amounts of acid albumen and hemialbumose are detect- able in the vomit and peptone is found in traces only. A further step then is, that these undigested proteids continue to remain in the stomach longer than with normal proteolysis. This means a much more prolonged burdening of the gastric walls, the stomach does not gain sufficient rest in which to prepare itself for the de- mands of the following meal, the distention by the weight of the food lasts longer. On the other hand much more of the carbohydrates will in this subacidity be converted into soluble starch, maltose and dextrose, than with a normal secretion of hydrochloric acid. With the pro- gressing stagnation and putrefaction of proteids, these products of starch inversion mean more ready food for bacteria, which are con- stantly introduced with the saliva, and finding in the moist and suitiable temperature of the gastric contents, congenial conditions for their development, the danger of progressive decomposition is very great. The toxic products of this carbohydrate and proteid decom- position, are irritants to the mucosa and increase the already exis- ting inflammation. When this inflammation has reached a certain stage an inflam- 6 — matory oedema of the muscular layers sets in, effectually destroying the, motility, and simultaneously as in most all serous and mucus inflammations an alkaline transudate exudes into the mucosa, neu- tralizing the last vestige of hydrochloric acid that may yet be sec- reted. Lactic, butyric and acetic acid are evolved from the fer- menting carbohydrates and further on H2COs and H. When this latter C02 gas and hydrogen begin to expand and the already impaired motility can not expel them by eructation, the stomach is still further distended. The normal hydrochloric acid not only acts as an antiseptic and antifermentative, but as we know undoubtedly, brings about energetic peristalsis, which effects a through mixing of the ingesta and frequently repeated contact and friction with those portions of the secretory membrane whose glands produce the hydrochloric acid and ferments. This mixing and triturating peristalsis is at the same time a most essential stim- ulus to absorption and ,eventually effects the timely expulsion of the chyme into the duodeuum. With impaired motility thereforcthe food masses remain too long in one and the same place. An intimate contact of the ingesta with the membrane as is produced by healthy peristalsis is essential for normal stimulation to continued secretion; hence the secretion of the oxyntic and ferment cells, already damaged by inflammatory infiltration soon ceases entirely. Resorption is not only impaired by absence of intimate contact with ingesta, but by the fact that the epithelial surface is in the various forms of gastritis covered with a tough glassy mucus, epithelial detritus, sometimes pus. In addi- tion to this, one must not overlook the element of the inflamma- tory changes on the rate, toncity, quality and quantity of the circu- lation on all of the gastric functions. The damaging effects of inflammation might be partly made up again by a healthy peristalsis, but as this is not present resorption and secretion suffer very much. The solution the resorptioh must be looked upon as an act of self protection as there are nothing but poisons to absorb ih these attacks. There is fortunately no excessive formation of peptone as this is prevented by the subacidity. So it is evident that in an acute gastritis there are numerous concurrent deleterious elements and changes, which are essentially similar to those of most light and severe gastric inflammations. — 7 - The clinical picture is a very manifold one as in the individual cases one may observe first one then another function that is most seriously damaged. It is natural to observe exceptions from the rule, thus in prolonged inacidity we may find cases in which the motility is unimpaired which of course favors intestinal digestion by timely evacuation of the chyme so that even the symptoms of dyspepsia may be lacking. ETIOLOGY. In the majority of cases, acute simple gastritis is caused by er- rors of diet. Irritation may be caused by quantity as well as quality of the food. Decomposed articles of liquid or solid nature will set up inflammation through the bacteria they contain. These germs must not be thought to invade the mucosa proper they exert effects by their action. Ewald (I.e.) says he has never found bacteria in the gastric tissues in these cases. Spoiled or decomposed meat, fish or vegetables, cheese, wine, cider or beer that has not comple- ted its fermentation, infected milk, impure pond water have been known to produce severe acute gastritis. Excessive indulgence in perfectly healthy food can provoke the trouble, not only by the mechanical distention and irritation which is caused thereby, but by the inability of the motor power to move the ingesta about and to expel them into the duodenum and also by the deficiency in the secretion of gastric juice which maybe able to digest a normal but not an excessive amount of food. The amount that can be digested tinder normal conditions without causing gastricismus will naturally vary considerably in different individuals. Chemical causes. Among these may be mentioned quinine salts in large doses, all metallic salts, particularly those of copper, antimony, arsenic, lead, gold and silver; acids and alkalies unless properly diluted. I have observed an acute gastritis follow the use of two grms. of sodium salicylate 3 times daily and feel convinced that iodide of potassium if not given properly mixed with food (right after meals) may lead up to gastritis. The various drugs used for gonnorrhoea internally. Cubebs, copaiba and the oil of santalwood may in susceptiable individuals bring about after long use a condition of the gastric mucosa in which acute gastritis is readily set up. ■ — 8 — Psychic causes. It is said that grief, sorrow, terror anger and even joy have been observed to produce acute gastritis. Sex- ual excesses particularly in neuasthenics are on record- as cau- ses. Thermic causes. Large quantities of very cold or very hot liquids can produce the disease particularly when taken in rapidly when the body is in an overheated state. mechanical causes. It is possible that pieces of fish bone. egg shells, oyster shell, fruit seeds if accidentally ingested may by mechanically scratching and bruising the mucosa cause a gastritis. I had occasion to observe a singular case of this disease in a pro- fessional base ball player by a blow from a base ball pitched with great speed. The bruise extended from the xyphoid cartilage to the left hyprochondriac region. The player was knocked sense- less and after partial recovery vomited a meal which he had taken two hours before mixed with blood and much mucus, later on he vomited some milk that was given him and on being tested this vomit was alkaline. The pain was so severe that morphine had to be injected hypo- dermically and food was kept out of his stomach altogether for 3 days during which period he was fed by Boas nutrient enemata. The attack lasted two weeks 'and patient made a perfect recovery. Predisposition. Manassein has shown that fever produced experi- mentally in dogs whom he had made anaemic by depriving them of much blood caused considerable suppression of the secretion of hydrochloric acid. And Kussmaul, Uffelmann, Leube and v. d. Velden have confirmed this subacidity in cases of fever in the hu- man being. It is therefore what we should expect to find if we de- tect developing gastritis in convalescents from severe diseases, also in tuberculous, cancerous and syphilitic patients. Functional gas- tric disturbances predispose to acute gastritis as well as pre-existing or concomitant diseases of the heart, lungs, liver and kidneys. Ewald believes in hereditary predisposition to gastritis as some families show numerous cases of the trouble in spite of the best care they take of their stomachs. Idiosyncrasy. It is a very perplexing fact that seme person in good health acquire acute gastritis after certain articles of food. Whilst I was resident physician of Bay View Asylum, I had a collea- — 9 gue, a perfectly robust vigorous man, who was not at all neuras- thenic and who developed this disease every time he ate oysters. He could not be induced to eat them at any time after he established the causal relation, but convinced as by consenting to an experi- ment. Influence of sex and age. Acute gastritis occurs more fre- quently in men than in women; of 36 cases observed by myself of whDm a record was taken, 10 occured in females and 26 in males. Females, during menstruation and puerperium are more frequently attacked. Old persons and very young feeble children are more easily to be attacked than those in middle age. In nursing infants a very slight change in the milk may be sufficient to cause it. According to Booker of Baltimore, acute gastritis in infants is accompained by prolongation of the time that the milk is retained in the stomach, at times over five hours, the gastric contents at times show epithelial and pus cells. Rotch, (Pediatrics, p. 854.) holds that the acute form is more common in infants and that the chronic form while it does occur in them is tmre frequent in children toward puberty. The frequent attack of gastritis occuring during the hot summer months are un- doubtedly largely due to the consumption of unripe fruit, Bou- veret, however (Trade des maladies de Pcstomac, p. 384, Paris, 1893-) attributes them to the abusive consumption of water. Accor- ding to Pick the disease has been observed to develope after taking cold. The effect of fever on the secretions of the stomach is not al- ways present. Edinger, in five cases of fever found the secretion of hydrochloric acid normal; having examined hectic, recurrent intermit- tent and typhoid fever patients. (L. Edinger, zur Physiol, u. Path. d. Magens. Deutsch. Archiv. f. Klin. Medtzin, Bd. 29 S. 555.) G. Klemperer (Dyspepsie d. Phthisiker Berlin, Klin. Wochsehr., 1889) and Schetty (Untersiich ii. Magenfunction bei Phthisis Deutsch Archiv f. Klin. Med., Bd. 44, S. 516.) confirm the finding of Edin- ger. Ewald (I.e. P. 301) found almost normal digestive power in a case of facial erysipelas. From these studies it is plain that not in all cases of secondary acute gastritis can we attribute the stomach affec- tion to the functional disturbances which the primary disease produ- ces, for in the first place these may be entirely absent, secondly the — 10 — frequency of the gastritis is not at all dependent upon the heigth or intensity of the fever. Thirdly the secondary sympathic gastritis may set in concomitant with the fever or even before it, ushering in the main infectious symptoms as a prodromal affection. The secondary sympathic gastritis is therefore more likely to be originated by localization of the specific, organized disease producers of the fundamental disturbance in the mucosa of the stomach or even by the toxic metabolic products of these microbes. In addition to the infectious diseases already mentioned, this sym- pathic form may be a consequence of diseases of the heart, lungs, kidneys and liver, causing venoys, passive congestion of the gastric mucosa (Stauungs Katarrh). In cardiac and nephritic diseases the passive gastric congestion may be relieved by appropriate medica- tion directed to the fundamental disorder, i. e. the use of digitalis, strychnin and diuretics. PATHOLOGICAL HISTOLOCY. According to Orth (Specielle Pathology. Anatomic, Bd. i. S. 702.) our knowledge concer- ning the pathological histology of the exsudative inflamma- tions of the stomach is very limited. In the first place, because uncomplicated simple acute gastritis rarely ends in death, and secondly, because post mortem changes and autodigestion exert a most disturbing and disfiguring effect in these superficial diseases particularly. In a case which M. Laboulbene observed, 24 hours after death by rupture of an aneurism, there existed hyperemia of the mucosa, localized ecchymoses, swelling of the mucus aveoli and augmentation of the mucus. Delafield and Prudden give essentially these same change's (Text book on Pathology) also Ziegler (Lehrbuch d. allg. und spec. Pathol Anat. Yena, 1890.) which may be summarized as follows; The surface of the mucosa is covered by a tough, glassy, cloudy or reddish mucus. The mucosa itself is injected -swollen and characterized by a hyperemia which is limited generally to the py- — 11 — loric region and rarely extends to the entire mucosa. Red spots either well circumscribed or diffuse are very evident and ecchymo- ses are scattered throughout the mucus membrane, larger sugilla- tions occur also but are rare. The histological changes are by most German authors said to be out of proportion to the degree and intensity of the syrhptoms (Fleiner I.e. P. 233.) That is to say they expect a greater extension and degree of inflammation to correspond to the severity of the symptoms, and are surprised not to find it. Fischl asserts this par- ticularly of the gastroenteritis of children (Fleiner I.e. P. 233.) However the exact and very instructive investigations of Prof. Wm. D. Booker (Johns Hopkins Hospital Reports, vol. vi, p. 159—258, Plates xvi to xxi.) show quite the contrary. Booker's researches demonstrate, destruction of the superficial epithelium in parts, infil- tration of the mucosa with polynuclear leucocytes, many cover (oxyntic?) cells are without nuclei and show only loose, granular protoplasm remaining. Epithelial cells and fragments of glands are collected in heaps on the surface, but not to so marked an extent as in the intestine (Booker I.e. P. 251.) In a few cases of acute gastritis associated with enteritis he found the entire gastric mucosa destroyed. Bacteriological cultures were made in 23 cases, in 19 the colonies were very numerous, in 2 moderately numerous and in 2 there were no colonies of bacteria, but many of orditim albicans. Tabulated his results appear as follows: Oidium albicans. Bacillus coli communis. Bacilli lactis aerogenes. Proteus Vulgaris. Streptococci. Booker, like A. Czerny and P. Moser conduces that the gastro enteritis of children is a general infectious disease with auto intoxi- cation in which other organs of the body participate, either as a re- sult of an invasion of the body by bacteria, as is often the case with the lungs, or from the effects of poisons absorbed from the gastro intestinal canal. This infantile digestive affection is undoubtedly a more severe and acute disease than any gastritis that occurs in adults, but its study certainly aids our knowledge of the allied dominant. Numerous. Few. Absent. Pure culture. Cases. Cases. Cases. Cases. Cases. 3 g 1 14 • 0 0 8 4 6 0 7 0 i) 7 2 >> 0 2 18 0 0 4 3 10 0 — 12 — pathological states of adults. There are a number of inflammations occuring in adults as well as children that are followed or preceded by digestive disorders, the etiology of which is much cleared up by the work of the authors above mentioned. I refer to the obscure attacks of parotitis, tonsillitis, pharyngeal abscess, sometimes fol- lowed well defined gastric ulcer and the disorders of the heart and nervous system concomitant or succeeding gastro intestinal lesions. These secondary attacks at times may be autointoxications, then again they show the unmistakeable signs of direct infection secondary to digestive trouble, for in the superficial epithelium is to be found the chief protection of the mucosa against the invasion of bacteria. When the epithelium is well preserved, bacteria are not found in the mucosa beneath, whereas they may be seen enter- ing it where the epithelium has been lost or injured. (Booker I.e.) The first step in the pathological process is probably an injury to the epithelium from abnormal or excessive fermentation in the stomach or from toxic products of bacteria and the many other con- ditions that have already been described. To prevent the effects of auto digestion and post mortem digestion on the gastric mucosa, Ewald suggested washing out the stomach immediately after death and filling it with alcohol. This may in future save a large num- ber of futile investigations. Formerly one depended largely on the studies of gastritis experimentally produced in animals for recogni- tion of the pathological changes. Thus Ebstein produced gastritis by injecting absolute alcohol into the stomach of dogs. *F,bstein. Ueber d. Veranderungen d. Magenschleimhaut durch F,inverleibung von Al- cohol u. Phosphor., Virchow's Archiv, Bd. 55, S. 469. I,osch. Ueber die nach Einererkung abnormer Reize auf die Magenschleimhaut auftre- tende pathologische anatomischen Veranderungden. Allgemeiue Weiner med. Zei- tung, 1881, No. 50. P. Grutzner. Neue Uutersuchengen uber Bildung und Ausscheidung des Pepsins im Ma- gen. Breslau, 1875. Edinger. Zur Kenntniss der Drusenzellen des Magens, besonders beim Menschen, M. Schultzer's Archiv, Bd. 17, S. 209. C. Kupffer. IJpithel und Drusen des mensch. Magens. MuncHen, I883. R. Virchow. Der Zustand des Magens die Phosphorvergiftung. Virchow's Archiv, Bd. 31, S. 388; Klebs. Handbuch d. Patholog. Anatomie, 1868, S. 174; Menassein, Chem. Bei- trage zur Fieberlehre, Virch. Arch., Bd. 55, S. 452; Ufflemann. Boebachtungen an einern Gastrotomisten. Deutsch. Arch, fur Klin. Med., Bd. 26, S. 441. Marfan. Troubles et lessions gastriques dans la phthisie pulmonaire. Paris, 1889; Stint- zig, Munchener med., Wochenschrift, 1890. A. Sachs Zur Kenntniss der Magenschleimhaut in Krankhaften Zustanden, Arch. f. ex- periment, Pathologie, Bd. 22, Heft 3, and Bd. 24, Heft 1-2. - 13 - Ewald and Ebstein describe a granular, cloudy swelling in the superficial epithelium. Whilst there is no differentiation possible between the parietal or oxyntic and the central, chief or ferment cells, both varieties are either swollen or contracted, granular, cloudy and with very indistinct nuclei. Between the different epi- thelia and in the interglandular connective tissue there are consid- erable masses of round cells. In these as well as in the imigrated leuccocytes and the cylindrical superficial cells numerous karioki- netic figures are very evident, and were claimed by Sachs [I.e.] to be characteristic for acute gastritis but this is denied by Ewald. Beaumont gives some strikingly correct descriptions of the conditions observed in the stomach of his patient Alexis St. Martin, when it was acutely inflamed in consequence of overfeeding or of abuse of alcoholic beverages. He states that the mucosa was mostly very hyperaemic even when no digestion was going on, swollen and covered with a thick layer of tough mucus. After ingestion the food was not digested but remained in the stomach from 4-6 hours. The secretion which was much diminished was only rarely weakly acid, mostly it was found alcaline or neutral. After a few days the mucus became still thicker but the hyperemia grew less. The fol- lowing account of Beaumont on the state of the mucosa in gastritis: "Its surface was marked with numerous white spots and vesicles like coagulated lymph, between which were very dark red spots:" Is con- sidered by Fleiner [P. 232. 1. c] and Fleischer [P. 802, I.e.] as un- intelligable in the light of our present knowledge. These remarks of the American pioneer of gastric pathology considered in that very light impress me as surprisingly acute and inspire the later days student with respect for the powers of observation in the man. Fisch, [Kleiner's Lehrbuch. p. 233] after what he considers very de- tailed and careful investigations, differentiates three forms of gas- tritis in children first, an interstital gastritts which he supposes to start from the connective tissue; secondly, a parenchymatous in- flammation having its seat in the glandular tubes; and thirdly, a combined parenchymatous interstitial inflammation. The intersti- tal affection may be interglandular or submucous also. Symptomatology and Course: Immediately after gross insults to the gastric physiology character- istic signs and symptoms appear. There are fullness in the epigastrium — 14 — which is distended and painful to pressure. Eructation, which at first may bring relief later on increases so as to be a great annoy- ance. Thirst, anorexia and even disgust for food may accompany this. The tongue is often thickly covered with a tenacious white fur, retaining the impressions of the teeth and colored by food or drugs, the breath is offensive. The secretion of saliva is augmen- ted, the pulse small and rapid. There may be painful contractions of the oesophageal musculature, spasmodic yawning and herpes labiales. A burning pain in the epigastrium which may radiate to the hypochondriac regions arises tinder the sternum (Pyrosis) toward the throat causing burning all the way and sometimes rais- ing sour or bitter stomach contents. As water and other liquids diminish the gastric burning, the patients usually show great thirst, the appetite however is absent or there is a perverse craving for piquante, acid or salty foods, whilst the habitual diet is detested. Taste is much disturbed. The nervous symptoms are general malaise, indisposition to mental or bodily work, prostration, cere- bral pressure and a frontal headache. Palpitation of the heart, gid- diness, a feeling of fear with profuse sweating are sometimes pre- sent. Nervous and less resistant patients (children) may have de- lirium. Fleiner declares, that general convulsions or loss of cons- ciousness are not rare in his experience. All these symptoms may arise directly from the stomach or reflexely from the central nervous system, which in these cases suffers intensely at times from the absorption of toxines from the stomach. If the nausea increases to emesis, there will be at first vomiting of food that has been eaten many hours before. This vomited material is mostly badly digested and imbedded in mucus. After emesis the symptoms may ameliorate and the nausea cease, very frequently however the vomiting continues when no more food is in the stomach. Then tinder much wretching saliva, mucus, bile and even blood may under great suffering be forced up. Intestinal parasites have in this way been forced into the stomach and vomi- ted up. Skoda first directed attention to cases in which vomiting was much impeded (at times prevented) by spasm of the sphincters, at the cardia particularly. If the last meals contained an abundance of carbohydrates or fats the vomited material will on testing show an abundance of — 15 - lactic, butyric and fatty acids generally; it will also contain acetic acid from the alcohol which was either the cause of all the difficulty or which in 9 cases out of 10 will be administered by laymen:— but the most characteristic chemical condition is the entire absence of free hydrochloric acid in the vomited matter, which is the cause of the perverse fermentations and decomposition in the gastric con- tents. The occurence of sulphuretted hydrogen in the contents of the stomach and in the urine which has been reported by Senator, in- dicates a condition of albuminoid decomposition which is extremely rare. State of the Urine. The quanitiy is as a rule diminished, in febrile cases the specific gravity is high and when constipation is present it contains an ex- cess of indican. Fever. Whilst about one half of the cases transpire without rise of temperature in the other half fever is present appearing suddenly and reaching at times 105° F. (40° Ct.) This form may in the be- ginning occasion some difficulty in the diagnosis because of its strong resemblance to developing enteric, (typhoid) fever. Some German writers still speak of Gastric fever as an infectious disease peculiar to itself (see F. Schmidt, dissertation, Berlin, 1885, Z. Frage. d. Existenz. d. Gastrisch; Fiebers, als einer eigenartigen Krankheit.) Though it is difficult to furnish proof of a direct infection in these febrile forms at present, it is not at all impossible that such a gastritis may exist. Future bacteriological studies in this disease may throw much light on this point. The fever of acute gastritis is usually preceded by repeated chilly sensations or by a typical shaking chill. Duration. If the rules of hygiene are regarded and the patient observes a careful diet, the disturbances will dissappear in 3 - 4 days entirely, there are of course much shorter attacks. The stomach remains very senstive to errors of diet, etc., for a varying time. A number ofneglected cases, or those occuring in very weakened individuals, may by a gradual transition turn to the subacute or chronic form. — 16 — The Diagnosis. In cases that are not accompanied by any fever there should be no difficulty in determining the nature of the disease, especially as the direct cause is in most instances apparent. The febrile form may be confounded with beginning enteric fever, during the first three days of the attack it may be impossible to differentiate the two. The existence of fever blisters (Herpes labialis) which according to Leo (I.e. P. 66) speaks against typhoid is in my experience an un- reliable sign, the results of the blood examinations are contradictory, and in the urine no diagnostic feature is known. The diazo reac- tion of Ehrlich even when performed in the originators latest meth- od (Charite Annalen 1886. B. ii). has in my experiences been of no diagnostic value. In this respect 1 can confirm the opinions of v. Yaksch and Eichhorst (Klinische Untersuchungs methoden P. 777). Most infectious diseases (see above) are in the beginning accompa- nied by an acute gastritis, in most of them particularly, the exanthe- mata a differentiation is not difficult. It is a good advice that v. Leube (Specielle Diagnose, 1 Theil, Leipzig), gives, when he says: "In all cases with high fever think of other sources and causes before set- tling upon gastritis". There are two conditions which as far as can be judged at present are reliable factors in the early diagnosis be- tween acute gastritis and enteric fever. (The early diagnosis is the only one I am here discussing, the element of time is very important here as simple gastritis is only of 3 days duration). And these are the manner and rise of the fever and the state of the spleen. In Enteric fever we mostly meet with a gradual rise of tem- perature and a gradual fall when the fever subsides. In gastritis the temperature rises abruptly, the remission are slighter and the fall is more sudden. (See Osier, Principles and Practice of Medicine, P- 349). Therefore frequent regular thermometrical studies are not to be omitted. The second diagnostic sign of value is the presence or absence of splenic tumor, its presence points to enteric fever. Un- fortunately the splenic enlargement is not invariably present in en- teric fever in the outset. The Prognosis. Speaking generally, the prognosis of simple acute gastritis— — 17 — except in very old patients and in young children—is favorable. The Treatment. 1. Prophylactic 2. Dietetic 3. Medicinal. Prophylactic treatment will especially be applicable to cases that are known to have enfeebled digestive organs or in whom at- tacks of digestive disease have repeatedly occured. Attention must be directed to avoidance of injurious influences that may affect the stomach directly from external causes and those that effect it from internal causes. (a) The external causes are of course the manifold varieties of trauma that are possible in modern life, not only those that can oc- cur accidentally but those that occur gradually by pressure upon the abdomen from without such as is requisite in the execu- tion of certain trades, the manipulation and handling of machines and even the continuous pressure of tables. A very important matter in this respect is clothing, particularly that of the female sex. Female clothing of today, as far as the maintenance of healthy digestive organs is concerned is not at all conformable to this object. The much condemmed corset is not even the worst part of the female outfit for a properly constructed and correctly "applied corset need not necessarily effect damage, however for the greater number of ladies wearing them it would be more hygienic to discard it altogether and preserve form and in sure support to the breast and graceful carriage in the style of the ancient Greeks, i.e. by broad, soft bandages applied immediately to the skin, over the underwear or even externally (Julia Marlowe Style.) A more harmful thing than the corset is the tying of the skirts and dresses around the waist. The most judicious female clothing conformable to the object of relieving the abdominal organs of pressure would be represented by garments made in one piece, of which the upper part supports the lower from the shoulders. (Kleinwiichter, d. Med.-Zeit., 1894, S. 82, also Meinert, Volkmann's Klin.Vortraege, 115, 116.) The abdomen should always be kept warm not by special ban- dages, but garments that are made of wool, fitting quite comforta- bly to the skin and closed below. All digestive sufferes should take special care against cooling or sudden chilling of the surface. (b) The internal causes of injurious influence must chiefly be — 18 - avoided in the food. Exclusive of corrosive and irritant poisons that may be swallowed accidentally the food articles may contain adulterations in form of organic or inorganic additions that are in- compatiable with sound digestion, or the food maybe decayed, fer- menting or decomposed. Among the adulterations might be men- tioned that of Milk with water, sodium carbonate and bicarbonate, borax, Salicylic acid, or it may contain bacteria (Tubercle and typhoid bacillus). Cheese adulterated with decomposable gelatines and may contain lead and tin from the packing, and also mineral impuri- ties. Sausages may contain flour, fuchsin, (for coloring) organic poisons, bacteria, ptomaines. (Botulismus poisoning by Sausage.) Butter may be adulterated by mineral substances, gypsum, lime, coloring matters, lead chromate, kresol and binitro naphthol. Vegetable Food; Flour has been found adulterated by sand, gypsum, alum, and also mixed with the fungi of the rye.or wheat—Ergot poisoning by rye flour has been observed in Russia, some confectioners use dye stuffs of various kinds all of which are dangerous. Coffee is sometimes adulterated with copper or lead salts to give it a desired color. Wine beer and whiskey are subject to numerous adulterations to effect cheaper manufacture, to preserve or color or give any desired taste. In beer, picric acid, colchicum and strychnin has been found as substitutes for hops, impure grape sugar for malt, alcalies to pre- vent souring and salicylic acid to preserve it or check fermentation. Furthermore the prophylaxis must be directed to the (1) qual- ity, (2) quantity of the food, (3) the proper preparation of the food by chewing and insalivation and proper conduct after eating. These subjects are best studied in works on dietetics: Gilman—Thompson. Dietetics. Wegele. Dietctische und Mcdicamentose Bchandlung der Magen und Darmkrankheiten. Penzoldt. Handbuch der Speciellen Therapie innerer Krankheiten, vol. iv. Beidert u. Langermann. Diatetik u. Kochbuch, Stuttgart, 1895. J. Btirney Yeo. Food in Health and Disease, Phila., 1897. Dietetic Treatment: Acute inflammation of any structure is best treated by rest and the stomach forms no exception (Tompson). Hence total abstinence from food and great reduction of the quantity of fluid imbibed is often curative after an interval of thirty-six hours. So, for the first two days as little food as possible should be allowed. To accom- plish this very simple and logical object is in private practice a most difficult thing. There is an incorrigible custom, among relatives to stuff the patient with all manner of articles, which is hard to combat. At the bottom of all of this probably lies the popular superstition that a human being can not exist twelve hours with- out food. A total abstinence from food is born very well and leads most rapidly to recovery. For the intolerable thirst, cracked ice should be given, a wineglass full in 2 hours. If there are signs of collapse, champagne or brandy can be added with safety even if alcohol was the cause of the trouble. After the 24 hours of total abstinence, the first food to be given is milk, beef bouillon with soft rice or an egg beaten up in it. A good stimulating food when there are signs of prostration consists of one raw egg beaten up with half a pint of Hocheimer or a full pint if desired and sweetened to taste with a slight flavor of lemon added. The wine may have to be diluted if the gastric mucosa is very sensitive. Of the above a wineglassfull may be given every 2 hours, (quite warm if preferred). On the third day a few soda crackers, or cakes may be allowed. On the fourth day a gradual return to more reconstructive food is advisable such as calfs brain free from all stringy and membranous parts, boiled first in bouillon then rap- idly broiled thereafter, sweet bread or thymusgland broiled, breast meat of broiled squab, pigeon or chicken. Finally, on the sixth day after the attack, finely scraped broiled beef, potato puree, stewed apples, rice, tapioca, very soft omelette. Medicinal Treatment: Acute gastritis must be treated without drugs wherever it is at all possible. If the dietetic rules of total abstinence from all food for 24 hours and cautious return to light diet are carried out, two thirds of the cases will recover without medicines. Not a few pa- tients, even children will do this instinctively and not permit any cramming with food until the stomach has become rested and a — 20 — natural desire therefore returns. The most important indication of treatment is usually done by the injured organ itself, i.e. evacua- tion. If emesis does not occur easily at the outset, both Ewald and Boas recommend the following emetic; Pulvis Ipecacuanhas, 1.5 Gr. xxiii. Antimonii et Potassi. tartratis 0.05 Gr. five-sixths. Sig. Misce. Fiat Chart, No. 1,—to be taken at once or in divided doses. In children, Ewald favors a teasponnful of the syrup of Ipecac I have so far been able to accomplish all that was necessary without emetics and loath to advise their use. Where emesis must be brought about it is more expedient and reliable to use % Gr. apomorphine hypodermically. Another drug which gives satisfaction to both patient and physician in this attack, particularly when there is constipation, is Calomel. Sometimes when persistent nausea follows thorough emesis it may even act as a gastric sedative. Ewald advises Gr. vi repeated in an hour. Whilst this dose seems large, it is by no means too large and will produce a cholagogue and infecting effect that may terminate the gastritis then and there. Formerly I used tablet triturates of Gr. y. of Calomel every hour until purgation, they are more pleasant to administer. The larger dose recommended by Ewald produces more of an antiseptic action since a portion of it is converted into the mercuric bichloride. Calomel can not be given at the beginning of the gastritis very weil, the second day is best suited for its administration. Although I mention these drugs it is not with a view to routine treatment but to aid in meeting special indications. When pain in the stomach is attended by chilliness, hot poultics over the entire abdomen, turpentine stupes or spongiopiline dipped into hot water and 10-20 drops of Tr. of opium sprinkled over before it is applied to the epigastrium. But when there is gastric pressure that seems to em- barrass respiration and associated with explosive eructation, cold hy- dropathic applications are more effective. When there is fever these applications should be made with ice water or the ice bag. Intense pain is met with hypodermic injections of morphine Gr. Y and atro- piae sulphate Gr. 1-150. The following suppositories of Boas can — 21 — R Codein phosphoric 0.05 Ext Bella dounae O.03 find application f. c Butyr. Cacao suppositor. N°x. One every hour until relieved. Where the pain must be relieved and the hypoder- mic injestion is not permitted and medication per os not retained. By the mouth Codeine is best given in the following manner; li Codeine phosph. 0.1 Sig. Aquae Menth pip. 40.0 One teaspoonfull every 3 hours. M. If symptoms of hyperacidity, keeping up the annoying pyrosis and thirst are predominant it may be impossible to avoid alcalies. They are epediently prescribed in the suceeding form. R Magnesia Calcined Sodium bicarbonaie a.a. 10. Menthol 0.2. Yl teaspoonful pro re nata. Mix thoroughly. It is not rational to give purgatives because they irritate the inflamed mucosa, Calomel is the only drug of this nature that can safely be given, but not before the fermenting stomach contents have been removed by emesis or lavage. To efiect purgation before the stomach is emptied, exposes the intestine to infection from the septic mass forced through it Persistent vomiting may call for especial treatment here morphine hypodermically, mustard plasters to the epigastrium and small pieces of ice will he sufficient. A singular case of very exhausting and persistent vomiting was in my practice relieved by Cocaine hydrochlorate Gr. y2 Menthol Gr. Aquae Camphor fl 3ss. M. every 2 hours until relieved. Vomiting of this character is bound to bring on collapse, it is for- tunately a rare complication but must be met energetically if it de- velopes. In concluding the Medicinal treatment I desire to refer to a succesful therapeutic measure which does not properly belong un- der this heading, because it is not medicinal, but mechanical. This consists of evacuating the stomach with the tube and im- mediately thereupon disinfecting it by washing it out with a solution of the following composition. R Thymol Gr. viii. Acid Boracic Iii. Warm water Oi (one pint). — 22 — The water during lavage must be used quite warm and the an- tiseptic not used until the plain water runs out clear. Catch up the outflowing antiseptic fluid and ascertain that it approximates one pint, a few ounces retained will not do harm. Vomiting as a rule ceases entirely after this. Six hours later wash out the color by large enemata of 20 i solution of Boracic Acid, no matter whether the patient has diarrhoea or constipation. If diarrhoea exists it is absolutely rational to effect the removal of the putrefying colonic contents by large enemata, (given in the knee chest position) and if constipation exists the stagnation of feces certainly aggravates the symptoms by increasing flatulence and abdominal pressure. If there is any therapeutic measure in addition to abstinence from food that merits confidence it is this mechanical cleansing of stomach and colon. Rare cases of high temperature may need special therapeutic measures for the fever; Here also drugs must be avoided and the temperature reduced by sponging with cold water or the cold bath. In case the appetite fails after the attack or there is protracted weakness with timidity and aversion to food, the following tonic may become necesarry. R Strychnin Sulphatis Gr. yi. Acidi hydrochlorici dilut. fl. sii. Elixir Gentianse qis ad Mis. fl. gvi. Sig. Misce. One tablespoonful Y hous before meals through a glass tube. PHLEGMONOUS OR PURULENT GASTRITIS — SUPPURA- TIVE INFLAMMATION OF the STOMACH — GASTRIC ABSCESS. THIS is a very acute, fatal ,and fortunately, very rare affection of the gastric walls apparently set up by an invasion of pyogenic cocci. It is a purulent inflammation invariably originating in the submucous connective tissue and from here extending to the mucosa. Ziegler ( Lehrbuch d. Allgem. u. spec. Path. Anat., 1887. Bd. ii. S. 516) describes large numbers of streptococci occuring partly free in the tissues and partly in the protoplasm of the cells. In case the serosa is invaded the disease as a general thing produces a general fatal peritonitis by perforation, unless an infection of the peritoneum is prevented by an agglutination with adjacent organs. 1 have never seen a case of this sort but as far as one is able to judge from the literature of this subject the disease is inevitably fatal running most always an acute, rarely a subacute course. Ewald (I.e. P. 303) has seen only one case and that at the clinic of his teacher Frerics. It occurs much oftener in men than in women; of 41 ca- ses 33 were men and 8 women. In a report by Glax, (Die Magen- entzundung Deutsch. Med. Zeit. 1884, N0.3) it is stated that but 51 ca- ses had been observed up to that time. Most authors that have had experience with the disease, distinguish first, an idiopathic pri- mary purulent gastritis, the etiology of which is obscure and second- 24 — ly, a secondary, metastatic phlegmonous or purulent gastritis which is an accompaniment or a sequence of other infections such as pyaemia, puerperal fever, anthrax, typhus or Variola. Anatomically one may distinguish a diffuse and a circumscribed purulent inflammation of the submucosa, the latter is spoken of as stomach abscess. Etiology; The direct cause of the rarer idiopathic phlegmonous gastritis is unknown. The predisposing causes may be the same as stated under the etiology of simple gastritis. The direct causes judging from anatomical specimens are undoubtedly bacterial invasions of the submucosa probably, principally, by pyogenic cocci, that find portals of entry through lesions in the superficial epithelium of the stomach, such as occur in most all gastric diseases, especially in so- called exfoliation in old ulcers or after trauma caused by fish bones, seeds, foreign bodies, etc., Ziegler's (I.e.) studies have already been mentioned. The secondary, metastatic phlegmonous gastritis which seems most frequent is that following puerperal fever and owes its origin to localization in the stomach of the specific organisms pro- ducing the fundamental disease. Whatever they may be it is self evident that only an enfeebled organ is liable to such an inflam- mation. Pathological Anatomy: The diffuse inflammation rarely invades all parts of the stom- ach with the same intensity, even if the whole organ is involved. The pyloric portion is generally invaded more than others; toward the cardia the inflammatory process is less and less marked whilst, the oesophagus is rarely attacked. The submucous layer is most extensively altered on cros-section, it is swollen showing an oedema- tous, purulent, or at times, a bloody infiltration. From here the in- flammation spreads along tlie interglandular tissue between the glandular tubules, effecting fine or larger perforations in the mucosa which may assume a sieve-like appearance. Pus wells up through these cribriform perforations as out of a swollen sponge. It may occur that the mucosa is lifted from the submucosa In.accumula- tions of pus. Rokitansky has decribed a case in which the mucosa was only strikingly anaemic, otherwise unaltered. Macleod (Lancet, 1887, vol. ii, P. 1166) describes a gastric abscess in which mucosa was said to be unaltered. — 25 — Toward the deeper portions of the engorged layers, the process spreads along the bundles of muscular fibers in the muscularis, which undergo fatty degeneration and show infiltration with pus cells and proliferation of nuclei. The serous or peritoneal layer may also be lifted from the subserous or muscular layers and perfec- tion as a rule rapidly follows inflammation of this layer. Circum- scribed abscesses which must be differentiated from the diffuse in- flammation are usually small, varying from the size of a hazlenut, to that of a goose egg (Leube I.e.). On cutting into the swollen elevated areas of mucous membrane, the abscess is found in the sub- mucosa but may extend through the muscularis to the serosa. Symptomatology; The symptoms are very much like those of a very intense acute simple gastritis; the pain of gastric phlegmon is not mater- ially increased by change of position or pressure. There is very rarely any vomiting of pus in diffuse purulent gastritis. Gastric abscess may be attended by copious vomiting of pus, after which a tumor that may have been palpable before, may become much smaller, or dissappear entirely; this phenomenon might be significant for the diagnosis of gastric abscess if it were not for the fact that pus tumors of the neighboring organs, sometimes break through into the stomach and cause the same symptoms. The fever reaches 104°-105° F., the patient being aware from the outset that he is very seriously ill. The sensorium is much disturbed by great restless- ness, headache, insommia, delirium. To the symptoms of acute gastritis those of a'sudden peritonitis may be added later on. Diagnosis: The important conditions for diagnosis are the pain, vomiting, meteorism, fever, diarrhoeas and general phenomena. The pain is localized in the epigastrium and said to have been absent in some cases. The emesis is always present and consists of pile, mucus and food debris, in diffuse purulent gastritis, pus has not been noticed in the vomit, which strongly resembles socalled peritoneal vomiting. The fever is very high and the temperature curve is said to re- semble those of pyaemic fevers with marked remissions and exacer- bations. Tympanitis and diarrhoea are more frequent than consti- pation. Other symptoms are, rapid compressible pulse, cold periphe- ral parts, hurried respiration, thirst and a much coated tongue. The — 26 — course of gastric abscess is not characteristic and Leube states (Spec. Diagnoied. Inner en Krankheiten S. 237) that the diagnosis is a matter of chance. The attack may resemble a circumscribed peritonitis or one of the various perigastric inflammations or abscesses, according to Ewald (I.e.) it may so mimic abscess of the spleen or left lobe of the liver, that a differential diagnosis is absolutely impossible. Deininger (Deutsch. Archiv f. Klin. Med. Bd. 23, S. 268.) held that high fever, constant and intense gastralgic pain that is not increased on movement, and increased resistance in the epigastrium, should be sufficiently characteristic to justify a diagnosis. These symp- toms however occur also in above conditions referred to by Ewald. Chvostek (Wiener Klinik,\ 881, and Wiener mcd. Presse. \877, Nos. 22-29.] however seems to have made the diagnosis in one of his cases. Where there is probability of diffuse or circumscribed phleg- monous gastritis, the exploratory puncture with an aspirating needle or the exploratory incision is in my opinion justifiable. In Penzoldt u. Stintzing's new Speciel Therapie Innerer Krankheiten, vol. iv. p. 446, von Heinecke gives suggestions for the operative treatment of phlegmonous gastritis. Prognosis is almost always unfavorable, especially in the dif- fuse form. After the circumscribed form, and evacuation of the abscess, several clinicans have reported recoveries, (Deininger I.e., Glax I.e., Kirchmann I.e., also Buckler, Idio. Path, phlegmon. Gastri- tis, Bayer, arztliches Intelligenzblatt, 1880, No. 37.) but it is im- possible to confirm whether they were really gastric abscesses. Dittrich has found cicatrices in the submucosa pointing to the possi- bility of healing. Treatment: If a diagnosis could be made it seems to me that these cases, the diffuse as well as the circumscribed forms, had best be treated surgically. Under the existing difficulty the treatment must be only symptomatic and limited to relieving pain by hypodermic in- jections of morphine, applications of ice, ice bag to the stomach, crushed ice by the mouth. To counteract collapse, wine enemata and hypodermic injections of strychnin are recommended. Medicines by the mouth are worse than useless. Infectious Gastritis — (Gactritis infectiosa, diphtheritica, crouposa, mycotica parasitaria). As Penzoldt correctly remarks. — 27 (I.e.) every gastritis is to a certain extent infectious, it is therefore that a number of authors reject the conception of infectious gastritis as a separate and distinct disease. Lebert (I.e.) and Osier (article on gastric diseases in Eulenburg'ls Realencyclopaedie 2nd edition, vol. 12, p. 410) believe that this is a characteric infectious gastritis peculiar to itself. Boas (Speciel. Therapie. d. Magenkrh. p. 6) is of the opin- ion that there is a form of acute gastro enteritis, well characterized clinically, which differs from simple gastritis by the gravity of the symptoms and particularly the course of the fever, so that it merits separate consideration. Ewald on the other hand holds that there is no sufficient specificity of inflammatory processes affecting the stomach for establishing a 'separate class of infectious gastritis. Fleiner, Penzoldt and Einhorn give no separate consideration to in- fectious gastritis. Those that establish a separate category for this affection class under this head all gastric invasions by infectious germs, so that all forms as remarked before are to a certain extent infectious. The symptoms are said to be very similar to acute simple gas- tritis and therefore require no further description. The course is more, protrated as it may last according to Boas 3-10 days, accor- ding to Lebert (I.e.), some case may have fever for 2-3 weeks. Gaffky (Deutsche med. Wochsehr. 1892, No. 14) gives an account of severe gastro enteritis in three persons who drank the unboiled milk of a cow affected with hemmorrhagic enteritis. Gaffky believes that the infecting germ was aparticulary virulent type of the Bacil- lus, coli communis. A number of similar mass epidemics are on record (Husemann, Deutsch med. Wochsehr. 1889. S. 960) that tend to strenghten the conception of a special infectious gastritis. There seems no necessity as yet for a seperate classification of this kind the subjest is still too hypothetical to be ranked as equal in impor- tance with other well characterized forms of gastritis. The diagno- sis, prognosis and treatment is said by Boas to be the same as for acute simple gastritis. Diptheritic gastritis is a rare affection, occuring not only as a sequence to Laryngeal and pharyngeal diphtheria but also as an accompaniment to pyaemia, septicaemia, puerperal fever, scarlatina, variola, endocarditis ulcerosa thyhus etc The disease is as a rule not discovered until the autopsy is made and for that reason has - 28 — more of a pathological than clinical interest. Mycotic Gastritis: When the vitality of the mucosa and the secretion of hydroch- loric acid has been reduced, suppresed or destroyed certain patho- genie fungi are known to invade the mucosa, producing ulcerations and necrosis. Most of these mycotic gastritic inflammations can not be recog- nized during life as such. Those that have been described are the authrax gastritis produced by spores or bacilli of authrax lodging in the mucosa or submucosa and giving rise to inflammation, ulcer- ation and necrosis. Sidney Martin observed a case of'anthrax of the anterior wall of the stomach at Guy's hospital, the primary infection was in the left check where a malignant purtule developed (Journal of Patho- logy and Bacteriology vol. i). Gastritis caused by the favus (fungus achorion Schonleinu) has been reported by Kundrat (u'ber gastro enteritis favosa Men. med. Blcetter, 1884 No. 49). The case was that of a drunkard whose gas- tric mucosa was predisposed by alcoholic chronic catarrh, he had favus universalis and in the stomach and intestines the fungi had caused diphtheritic inflammations, with fibrinous exudations, ulcer- ation and sloughing, death was caused by a terminal colitis it ap- pears. The thrush fungus German-Soor Latin-oidium albicans has been reported as setting up a mycotic gastritis; in some cases of which the stomach alone appeared infected, throat and oesophagus were intact. The yeast fungus (Torulae or saccharomygces cerevisiae) sarcinae, the common moulds (Penecillium Glaucum and Mucos) and various schizomycetes occur in the gastric contents and set up irritation of the mucosa not by direct invasion it appears but by the toxic pro- ducts of the fermentation which they cause. Sarcinae according to Hiihne do not bring about any fer- mentation. Miller's interesting investigations concerning the bacterial flora of the mouth have been refered to on page 41. In the first volume of his excellent text book (Specielle Pathol. Anatomie B: 1, p. 704). Johannes Orth describes an interesting bacteriae invasion near an — 29 — old chronic gastric ulcer which had largely become healed. At seve- ral places there were grayish, bran like incrustations partly adherent which anatomically had to be designated as diphtheritic. In the scabs or crust and in the deeper parts of the mucosa, and partly, lodged distinctly in lymph vessels, were numerous bacilli that had some morphological resemblance to those of anthrax, this suppo- sition could however not be confirmed by cultures. The case was complicated by the fact that a fatal hemorrhage had occured from a very small arteriole at a place where only a very tiny defect in the mucosa was observable. In the immediate neighborhood of this defect the bacilli were found also but not insufficient numbers to attribute to their destructive agency the tearing of the arteriole which was not aneurism atic. Orth then proceeds to refer to the bacillus gastricus or poly- sporus brevis of Klebs (iiber infectiose magenaffectionen Allgemein. Wien. med. Zeit. 1881, No. 29 and 30) which was found free in the lumen of the glands as well as between the cells of the glands and the tunica propria; there was also an interglandular small round cell infiltration. Bottcher (Dorpatcr med.Zeitchr. 1875, p. 184) also defended the view that gastric ulcers are in part due to mycolic and bacterial in- vasions. Unfortunately Kleb's and Bottcher's statements have not been confirmed by later investigators. Animal parasites are also on record for producing gastritis; C. Gerhardt (Magenkatarrh durch lebende dipterenlarven Jenaer med. Zeitschr. Bd. 3, S. 522) gave an account of acute gastritis set up by larvae (maggots) of diptera, a class of insects of which the com- mon fly, the flee, etc., are examples. The egg of these larvae were said to have been swallowed with rasberries. Meschede (Ein fall von Erkrank. durch im Magen weilende lebende Maden Virchow^s Archiv, B. 36. S. 300) reports gastritis caused by maggots eaten with cheese. Senator reported gastritis set up by living maggots of the common fly which occured in the mouth and stomach (Berlin Klin. Wochenschr. 1890 No. 7) the same observation was made by Hildebrandt (Berlin Klin. Wochenschr. 1890, No. 19). Fermaud ob- served a case of gastritis and gastralgia caused by an earthworm (Journal de med. practique de Paris, 1836, tome vii. p. 57). It is known also that ascarides and tape worms may reach the stomach - 30 - in rare cases and give rise to severe inflammations, which may sub- side at once as soon as the offending parasite is vomited. Toxic Gastritis: (gastritis venenata) This form of acute gastric inflammation is caused by poisons or corrosive chemical bodies. The poisons that have been taken either by mistake or suicidal intentions are mercuric bichloride or corrosive sublimate, phosphorus, arsenic chloroform, creosote, potassium chlorate, oxalic acid, nitrobenzol, carbolic acid, the concentrated inorganic acids, sulphuric, hydrochloric and nitric acid. The caustic alcaline hydroxides in strong solution, and futhermore alcohol in all its forms and some substances used as medicines and (see etiology of acute gastritis) particularly croton oil and antimonium and potassium tartrate (tartar emetic) also ammonia. The Pathology will necessarily vary considerably as it is not only dependant upon the kind but also upon the quantity and concen- tration of the poison, or upon the circumstance whether the poison is taken on a full or empty stomach as food and drink dilute the drugs. There may be only a very slight superficial inflammation or a very penetrating corrosive effect, involving the entire gastric wall and even leading to perforation. Different drugs produce dif- ferent efiects upon the mucosa. Phosphorus, arsenic antimony and alcohol produce in excessively large, toxic doses a milky, yellowish white or opaque appearence. The epithelia of the alveoli of the tubular glands are partly in a state of mucoid degeneration, partly finely granulated, cloudy and showing fatty degeneration; the same is the case with the secreting cells. The tissue between the cells is crowded with a small round cell infiltration. In this condition auto- digestion by the gastric juice may cause peptic ulcers i.e. when the poisons are not taken sufficiently strong to effect ulceration or to destroy secretion. Dilute acids and alcalies induce the pathological picture of a simple acute gastritis, whilst in concentrated form, a deeply pene- trating necrosis with formation of crusts and intense reactive in- flammation with serous infiltration, suppuration and blood extra- vasation are the result. The scabs or crusts show different colors with different corrosives. Under the effect of sulphuric acid they are black, of nitric acid yellow, of alcalies brown, of coppersalts - 31 - green or blue, of silver salts black. Dislodgement of these crusts leads to fatal bleeding, tearing off the serosa or perforation with peritonites. Oxalic acid is said to produce a jelly like swelling that is semitransparent, ammonia causes a pustular one. Symptoms: After taking the poison there is generally indescribably severe pain, intolerable burning, vomiting which increases the pain and causes fainting at times. The vomit as a rule contains blood or bloody mucus, the thirst is great. There is most frequently diarr- hoea containing blood. Severe general symptoms follow, small very fast pulse, jactitation delirium. In case much of the poison has reached the general circulation, haematogenous icterus, petechiae albumimuria and haematuria may follow. Death follows in a few hours or few days from collapse or later by perforation peritonitis. Even if the patients are tided over the first period of acute gastric symptoms, they may die later in from hemorrhage when the scabs and crusts are sequestrated or by the consequences i.e. stenosis of the oesophagus, cardia, pylorus or atrophy of the mucosa. The Diagnosis after knowing the history of the case will not be difficult. One should not fail to make a thorough examination of the mouth and throat where the corrosive effect, if any, will be evi- dent. An analysis of the vomit will probably inform of the nature of the poison. The Prognosis of severe toxic gastritis is necessarily fatal if not by the direct poisoning or first destructive effect of the drug, cer- tainly by the severe secondary effects. The Treatment will vary with the nature of the poison. In recent poisoning with strong acids magnesia tista, (calcimed) should be given as soon as possible, if no drugstore is near, give chalk or even powdered lime which can be scraped from the wall. Whenever possible the stomach tube should be at once used for all poisons, of recent date. Boas, Fleischer and Pick advise that it should not be used in severe acid or caustic alcaly poisoning because of the danger of perforating the stomach. As most such cases will probably die of perforation anyway, I certainly should use the tube and let the pa- tient take his chances. A large quantitily of water with sod bicarb in case acids were taken or vinegar in case alcalies were taken, will - 32 - doubtlessly dilute and combine with the destructive agent present. Lemon juice will also answer for the alcaline caustics. In all other poisonings the stomach tube, or if convenient the pump should be used as soon as possible and the stomach washed out thoroughly. For other poisions the approved antidotes should be given (freshly prepared hydrated oxide of iron for arsenic, etc.) that will be found in various text books on toxicology and therapeutics; H. A. Hare's system; H. C.Wood; Lauder Brunton; Binz, Schmiedeberg; Penzoldt and Stintzing's system vol. vi. After carbolic acid ingestion, wash out, and then pour in olive oil 250 c.c. In all corrosive poisoning cases the pouring in of olive oil or molten vaseline, after neutralization and washing out, will if possible, diminish the corrosive effect. Where not too much acid or alcaly has been taken, the subnitrate of Bismuth or subgallate of Bismuth, z\ t.i.d. if possible, swallowed with oil will favor rapid circatrization and inhibit bacterial infection of the necrosed, charred areas. A suspension of Bismuth stibnit. § i. to one pint mucilage and water has proved advantageous in a case of carbolic acid poisoning in my practice. If the pain is severe, morphine hypodermically in Y to Y grain doses repeated until relief comes. It is our duty to give re- lief to the pain at any risk, even if chloroform anaesthesia is requir- ed; for after the suffering ceases our efforts to save the patient can be more easily executed. Nutrition must be carried on by rec- tal enemata only. By the mouth, ice is about all that is permissi- ble; it will tend to diminish the pain, fever and inflammation. I make such an explicit statement of treatment because I had experi- ence with two cases where the autopsy showed that recovery might have been possible as not mueh sulphuric acid had reached the stomach if the treatment had been more heroic i. e. if the tube had been used for timely romoval of the poison. CHRONIC GASTRITIS. MOT much over a decade ago it was customary to class all Ii stomach diseases that were not acute and that could not be ' diagnosed as dilatation, ulcer, or carcinoma, under the head of chronic gastric catarrh. With Ewald and Penzoldt, I agree in their objections to the word catarrh and the reasons have been given under the chapter on simple acute gastritis. Even at the present day there is no absolute uniformity on the conception and limitations of the word chronic gastritis. With the aid of improved methods of diagnosis, particularly such methods as permit of an exact study of the various gastric functions, the socall- ed gastric neuroses have been recognized as separate and distinct diseases, formerly they were believed to be symptoms of chronic gastritis. This chronic inflammation of the mucosa affects all of the important functions, although one or the other of these is generally most seriously affected There are observed many variations of the kind and intensity of disturbed function, from a trivial reduction of secretion of gastric juice or interference with motility to com- plete suppression of glandular activity and pronounced insufficiency of the peristalsis There are two pathological processes that appear as conditions to every chronic gastritis; these are desquamation and — M — degeneration of the glandular cells and infiltration of the connec- tive tissue. Bearing in mind these conditions we may distinguish two main types of chronic gastritis, first the hypertrophic, and secondly, the atrophic. The hypertrophic form consists of proliferation of the connec- tive tissue leading to change of form and folding or warty elevations of the mucosa (Etatmammelonne or polyposis). The end of this pro- cess is a complete destruction or cystic degeneration of the glands. A grayish brown or in places a dark red brown color is peculiar to this swollen and proliferated mucosa, which is covered with an ad- herent gray coating of mucus. The atrophic form consists of contraction of the connective tissue, loss of .the epithelium and more or less complete destruction of the glands, in rare instances, superficial ulcerations. The mu- cous membrane is much thinned out, very smooth and of a gray- ish white or pale slate gray color. If the process attacks the mus- cularis and submucosa it may cause atrophy of the muscle fibrils, with or without thickening of the entire gastric wall due to connec- tive tissue new formation. Then again we may meet with a genu- ine hypertrophy of the muscularis, particularly at the pyloric por- tion or in the pylorus itself. The lumen of the stomach in these forms may show a normal capacity. Or it may be much diminished in size by connective tis- sue thickening of the gastric walls and subsequent contraction, this is known as gastric cirrhosis (Brinton) and may reduce the normal capacity to one of 160 c.c (Leube, Penzoldt). Or again, the capacity is much increased by a dilatation in consequence of chronic gas- tritis and hypertrophic pylorus stenosis. So the anatomical picture may present, atrophy of the mucosa with wasting of the tubular glands and of the muscularis, thinning of the entire gastric wall and very frequently dilatation, or on the other hand, inflammatory hyperplasia of the layers of the stomach with excessive connective tissue proliferation leading to cirrhosis ventricul hypertrophic pylorus stenosis, atrophy of the glandular layer and sometimes of the muscularis. This form may lead to marked reduction of the lumen or more frequently if a stenosis exists, to a dilatation. Both forms - 35 - bring about grave disturbances of motility, secretion and absorp- tion. The cause of the elevated, warty or polypoid projections of the glandular layer is to be sought in the fact that in certain forms of the disease the mucus layer grows much more rapidly than the submucus layer, bringing about a rough, wrinkled, mammillated surface that has been described as gastritis polyposa, and by some French writers is termed etat mammelone. (See Orth, Specielle Pathol. Anat. bd. i, p. 709). A number of Germans describe a variety of special forms of chronic gastritis under the names of Saurer Ka- tarrh—sour or acid gastritis, Schleimkatarrh—slimy or mucus gas- tritis, also termed gastritis atrophicans and a simple chronic gastritis or Einfacher Katarrh. All of these terms are quite unfortunately invented and unscientific because they are artificial. The so-called Saurer Katarrh is not a gastritis at all, (Ewald) but a neurosis of secretion, a hyperacidity and the result of secondary irritation of the mucosa. Etiology Chronic gastritis is a widely spread disease occuring in all stations of life but more frequently among the poorer classes where the quality of the food is so inferior as to keep the stomach in a constant state of irritation. All the numerous injurious influences which arise from a defective and inappropriate diet have been re- ferred to under the head of the pathologenesis of acute gastritis. It may evolve out of the acute or subacute form as the mucosa has been damaged by the altered circulation and its resistance to disease lessened. All processes that lead to venous congestion of the stom- ach, i. e. affections of the portal system, especially of the liver and spleen, also diseases of the heart may cause it. There are certain con- ditions which may bring about chronic gastritis by effecting alterations in the composition and structure of the blood, these are anaemia, chlorosis, scrofula, secondary anaemias following typhus and ty- phoid fevers, the exanthemata, pregnancy, tuberculosis, diabetes, gout and Nephritis. Irritating substances brought in contact with the mucosa continuously either from without or within i. e. from the blood are believed to cause the disease. Ewald states that it may result from direct local irritation and neoplasms. My experience is that in the vicinity of such structural changes pre-existing in the mucosa, there is indeed a gastritis observable but it mostly partakes 36 - of an acute or subacute type. The defective chewing and insaliva- tion, hurried eating and swallowing of large pieces of food, putre- faction of the mouth from carious teeth or the manifold forms of stomatitis and gingivitis. In this country the excessively hasty eat- ing and the abuse of ice water with meals and of tobacco and alco- holic liquors between meals are the causes of the frequency of chronic gastritis. The American people residing in cities live for a large part un- der commercial and social customs that are pernicious to the diges- tive organs. Foremost, among these conditions are the high men- tal pressure under which the demands of business are carried on, the constant worry, nervous tension caused by force of com. petition. The anxiety to get rich rapidly by straining all mental and physical powers to make the utmost possible gain, all these things bring about a hasty, nervous manner of taking food, chewing is a process which most business men execute in a perfunctory manner only. There is no-time for insalivation, if they could they would gulp the food down dry, as it will not go down that way they help it down with ice water. Tobacco juice is responsible for much of this disease, also condiments used habitually, pepper, ginger, mus- tard, horse raddish and the habitual use of drugs (arsenic, silver salts.). Chronic gastritis is the most frequent disease among habitual consumers of alcoholic liquors. From what was said tinder acute gastritis of the experimental production of this disease with alcohol by Ebstein, the frequency of the chronic form among the devotees to Bacchus and Gambrinus is very intelligible. As Ewald correctly remarks the disease may be classified among those in which the pa- tient's indiscretions play a very important role. But as most per- sons treat their stomach badly and neither eat with proper mastica- tion and insalivation, nor are able to resist culinary temptations, gastritis is one of the best nourished and most prevalent diseases in the world. "Indigestion is the remorse of a guilty stomach" says Ewald and F. Albin Hoffmann (Vorlesungen ueber allgemeine Therapie Leipzig, 1855.) expresses a sentiment that deserves to be an apothegm — "^eber 2Henfdj f)ctt ben SWagen ben ev 311 fjabeu r>evbteiit„ — "Every one has the stomach which he deserves." It is not intended - 37 to do injustice to a large number of sufferers from weak stomachs who take the greatest possible care to avoid dyspepsia and never- theless are liable to acute or chronic gastritis. The etiology explains why the male sex is affected much more frequently than the fe- male. The Pathological Anatomy: These changes are as in the acute form, most pronounced in the pyloric region and from here extends to the fundus. The alter- ations of structure occuring in the course of chfonic gastritis pre- sent varying pictures according to the duration of the disease. In the later stages the variations are considerable, since at this period the consecutive changes may one time incline to inflammatory hy- perplasia, at another may show an atrophic character and also be- cause either the mucosa or submucosa only or in other instances the deeper layers may be involved with alternating intensity and extent. The inflammatcry process is not at ail limited- to mucoid de- generation and desquamation of the surface epithelium but pre- eminently affects the glandular elements and interstitial tissues and from here attacks the deeper layers of the gastric wall. In early stages there is a general diffuse redness, in later stages this color that is due to hyperaemia gives way to a peculiar pigmentation which first assumes a bluish or brownish shade and finally gets to be of a dirty red brown or slate gray or both. This pigmentation is generally limited to the pyloric region but in spots it may be spread over other sections of the inner surface of the stomach. The color is due to blood pigment which has become stored up in the cell and intersti- tial tissue; also to blood corpuscles that have left the vascular chan- nels and undergone pigment metamorphosis during the long stan- ding chronic hyperaemia. This pigment action must not be con- founded with post mortem discoloration. Inflammatory Hyperplasia: !n this form the gastric mucosa may either preserve the velvety appearance that is peculiar to the normal inner surface of the contrac- ted stomach or it may be covered with irregular warty projections and exhibit immense development of the pyloricplicce villosce; this is due to inflammatory infiltration of the interglandular and subgland- ular connective tissue, but particularly to the same process occur- _ 38 - ing in the connective tissue ridges present between the vestibular entrances to the gland ducts ( Vorraume of the Germans], or peptic duct alveoli as I prefer to call them. If these hypertrophic — hyperplastic processes are confined to circumscribed spots, they may assume exaggerated degrees forming polypoid proliferations, which as a rule are attached by broad bases, but in consequence of connective tissue contraction they may occur pedunculated. In this way papillomatous excrescences may be de- veloped which project into the lumen of the stomach (gastritis poly- posa, Orth, I.e. p. 716). When the submucosa is attacked with in- flammatory infiltration and connective tissue new formation, the loose tissue is first transformed into one much richer in cells and then in- to a tougher, more inelastic layer resulting naturally in a much re- duced movability of the mucosa upon its substratum. When this chronic processs leads to cicatricial contraction in the hyperplastic submucous tissue it may lead either to partial, localized change of form or to a more or less general, uniform contraction (SchVump- hung, cirrhosis ventriculis. Linitis plastica, Brinton). In the pyloric portion this process may lead to stenosis. Frequently the muscu- laris is hypertrophied as a consequence of the chronic irritation transmitted through the submucosa, this muscular hypertropy is most pronounced at the pylorus. This localization of the maximal intensity of the inflammatory process in the mucosa, submucosa and the muscularis at the pylo- rus makes the origin of a pylorus stenosis in consequence of chronic gastritis intelligible. This kind of a stenosis is usually spoken of as benign, in contradistinction to the malignant stenosis of carci- noma. Much deversity of opinions exists concerning the origin of the etat mammelone (Mammelon means the nipple of the mammary gland. Frerichs held that it was due to accumulations of fat in the mucosa and inflammatory hyperplasia of the lymph follicles contained in it. Rindfleisch's view was a greater increase in growth of the mucosa than in the submucosa. Ziegler explained the mu- cosa polyps by proliferation of the submucosa. Ebstein assumes an inflammatory hyperplasia of the tissue between the glands, Jones believes in an excessive contraction of single bundles of the mus- cularis mucosa as a cause. Undoubtldly this gastritis polyposa 39 - with its mammelonated appearances may be formed by a variety of very different processes. INFLAMMATORY ATROPHY: The progressive plastic character of the inflammation just de- picted may lead to a retrograde metamorphosis before it has pro- gressed very far, in some cases it may not develope at all but the disposition to break down and atrophy may start early in the dis- ease. These atrophic changes are most marked in the glandular ele- ments and may be limited to these. Sometimes the inflammations of the mucosa and gland cells have a degenerative tendency from the outset and no hypertrophy or hyperplasia enter into the anato-. mical picture. The surface columnar epithelium and the cylindrical epithelium of the vestibular alveoli falls prey to a mucoid degene- ration and desquamation. The epithelial cells of the peptic glands undergo a fatty degeneration. During this atrophy the mucosa changes to a thin, smooth, pigmented or slate gray membrane. This atrophy may be limited to the mucosa while at the same time hypertrophic processes go on unhindered in the submucosa and muscularis, then again the atrophy may extend to the latter layers and bring about a wasting of all gastric layers, this was formerly spoken of as Taber of the Stomach, the Phthisis ventriculi of Roki- tansky. Under these irrepairable atrophic states anomalies in the gastric volume may develope but dilatation is more frequent here than contraction. Atrophy of the stomach may occur without preceding chronic gastritis, it then takes the character of a simple degenerative pro- cess and follows severe anaemic and cachectic states and also grave infectious diseases and poisonings. When confronted with cases of gastric atrophy with absence of hydrochloric acid the ferments and enzymes and coexistant anae- mia it is sometimes very difficult to decide which is the primary causative disease. In these cases it is well to bear in mind that anae- mias, even those of a grave pernicious character are much more of- ten a consequence of, or rather secondary to atrophy of the gastric mucosa. Our countryman Austin Flint was fhe first to call atten- tion to the relation between anaemia and atrophy of the gastric glands. In i860, (Austin Flint,'American Medical Times.) he ex- pressed the opinion that some cases of obscure and profound anae- — 40 - mia are dependent upon degeneration and atrophy of the glands of the stomach (further contributions of Flint to this subject are to be found in the New York Medical Journal, March 1871, and in his Principles and Practice of Medicine, p. 477, Phila., 1881). Since Flint's publication, cases have been reported by Fenwick, (The Lancet, \877, July, etseq) Quinke, ( Volkmannh Samml. Klin. Vortrage, No. 100, caseb.) Brabazo, (British med. Jour., 1878, July 27) Nothnagel, Deutsch. Archivf. Klin, med., Bd. 24, p. 353) Bartel's, (Berlin Klin. Wochsehr. 1888, N0.3) Scheperlen, (Nordis. med. Archiv, 1879, Bd. xi, No. 3) Osier, (Atrophy of the stomach with the clinical features of progressive pernicious anaemia, Am. Jour. med. Sciences, 1886, No. 4). Rosenheim reported two cases which appeared to be pernicious anaemia (Berlin Kim. Wochsehr. 1888, No. 51r52.). Inasmuch, as these cases of atrophy of the gastric mucosa are accompanied by marked changes in the blood, signs of break down in the red blood corpuscles, increase in the white and formation of macrocytes and microcytes, the question may arise whether pernici- ous anaemia is really an independent disease or is the result of gas- tric atrophy (Ewald 1. c.). Atrophy of the mucosa that is not secon- dary to well-known stomachs or general diseases but occuring as a primary disease has been claimed to exist by Fenwick I.e. The impression might be gained from the statements of some writers, that the hypertrophic hyperplastic form of chronic gastritis may change into the atrophic form from its fully developed stage. This would mean the total dissappearance of the papillary, poly- poid proliferations of the etat mammelone, because the mucosa of the atrophic form is very smooth. This, according to Orth (I. c. p. 710) is very improbable, for he is of the opinion that the atrophic form is developed uniformly by transformation of cellular intersti- tial tissue into contracting cicatricial tissue, bringing about thinning of the mucosa and degeneration of the glandular elements'without the intervening of hyperplasia above referred to. Ulcerative processes are said to occur (Ziegler I. c) when in the course of the disease, intense (hemorrhagic) inflammation effects necrosis of the epithelium and submucosa and its subsequent seques- tration. In this way the so-called catarrhal gastric ulcers and hem- orrhagic erosions are formed, which may be associated with hem- — 41 - orrhage. Cruveilhier (Anatomie Pathologique du corps Humaine) terms it a follicular gastritis, in which ulcers are said to originate in the follicular glandular apparatus. The catarrhal gastric ulcers of chronic gastritis are mostly small, round or irregularly indentate. They are supposed to healand form flat, pigmented cicatrices. Forster asserts that they may lead to perforation. Orth I.e., whose statements merit confidence because of the scientific conser- vatism of the man, is of the opinion that ulcerative processes in the course of chronic gastritis are very rare. The Pathological Histology: The minute anatomy of the process is that of a parenchymatous and interstitial inflammation, perhaps the most graphic description of it is given by Ewald /. c (translated by Morris Manges, New York, 1892). The cells of the peptic ducts are described as being partly totally destroyed, partly granular and partly shriveled up. Differentation between the central, chief or principal cells (Hauptzel- len) and the parietal, border or oxyntic cells (Belegzellen) is impos- sible. Osier and Henry /. c. ( also in the Principles and Practice of Med. by Osier) describe a case in which the greater portion of the lining membrane of the stomach was converted into a perfectly smooth articular structure, showing no trace of glandular elements, but enormous hypertrophy of the muscularis mucosa and forma- tion of cysts. Symptomatology: As a general rule the outset of chronic gastritis can not be deter- mined with certainty, because it developes very gradually and insid- iously either as a continuation of acute gastritis and of other diseases or as an independent disease, and because the initial symptoms not being very pronounced are generally disregarded, only the sudden aggravation caused by dietetic errors and other injurious influences lead to the recognition that a serious disease is present. The clini- cal picture varies considerably, although the signs of a disturbed digestion as indicated by dyspepsia, absence of appetite, eructation, nausea, vomiting, pressure and fullness in the gastris region, repeat themselves in various cases, first one symptom and then another will press to the foreground or be absent entirely. Perhaps the most constant of the early symptoms is absence of appetite. — 42 — Absence of Appetite — Anorexia: Even in the less serious attacks, this as a rule is present and may be aggravated to a disgust for the customary diet. Taste: I have rarely observed a case of chronic gastritis in which there was not present a pharyngitis, posterior nasal catarrh, laryngitis or one of the forms of stomatitis, one or other or several of these, usually the latter. This condition of the mouth renders taste per- verted, pasty sometimes distinctly offensive, acid, bitter or metaL lie NAUSEA is an early symptom, generally preceding emesis; but it may exist by itself for many hours without emesis and may even occur on an empty stomach. Eructation is present at some time in all of the cases, the gases that are brought up are either air or carbon dioxide or hydro- gen, in some rare cases inflammable gases, marsh gas CH4 for in- stance have been eructated (Ewald — Rupstein). Vomiting, though not so frequent as in acute gastritis, is never- theless quite frequent. In the chronic gastritis of drinkers it is of- ten a regular occurence every morning and then known as the mor- ning vomit or vomitus matutinus, which Frerichs used to explain by the swallowing of the secretions from the pharyngeal catarrh and saliva during the night. The morning vomit is usually alcaline, in- verts starch to sugar and gives the red rhodankalium KCNS reac- tion with chloride of iron. In beginning and in not very grave cases the ferments pepsin and rennin are yet to be detected, but in later stages only hydrochloric acid slightly in excess of the deficit will demonstrate the ferments; this really shows that the proenzymes, not the perfect ferments are present.. Finally, pepsinogen and rennet zymogen are absent in very advanced forms, even the mucus will cease to be secreted; this is an indication of the complete atrophy of the mucosa. The Tongue is very frequently coated with a grayish white deposit most mark on the back and root of the organ. The im- pressions of the teeth are retained by it. At the edges and apex the tongue appears in a deeper red color with swollen papillae. The coating may dissappear toward evening to reappear in the mor- ning. Henoch (Klinik der Unterleibs Krankheiten, Berlin, I863, p. — 43 - 382) holds that the appearence of the tongue is really not always a mirror of the stomach but that its condition is to be regarded simply as an index of the existing state of the oral mucus membrane. Certainly the tongue is much more frequently the first organ to be- come diseased of the two, as it is nearer the outer world and its in- fections than the stomach. Therefore it might be supposed that catarrhal states of the tongue, mouth and throat may occur more frequently as independent diseases not secondary to diseases invol- ving the stomach, than as secondary diseases extending from an antecedent disease of the latter. Schech, (Krankheiten d. Mund- hcehle,) in addition to malformations and inherited or acquired form defects of the mouth, describes sixteen distinct diseases of the hu- man mouth not including neoplasm, tumors and nervous diseases; and Seifert (Penzoldt and Stintzing's Handhuch der Speziell. Therapie, Bd. iv.) describes 23 mouth diseases. In the primary form all of these arise in the mouth and occur as secondary forms in acute inflammatory conditions of the digestive tract, particularly after infestious diseases. I have paid particular attention to the state of the tongue, oesophagus and stomach at autopsies, and also during a large number of analyses of stomach contents, and must admit that the condition of the tongue is one of the most variable signs in gastric symptomatology. The cases of manifest disease of the stomach where a primary disease of the mouth is out of the question are extremely rare. By a critical review of the etiology of gastric dis- eases, one can not fail to be impressed with the fact that the promi- nent causes can and most often do affect the mouth and the stom- ach alike. The gastric disorders in which the tongue is most fre- quently unaffected are those associated with little gastric sepsis, i.e. ulcer, hyperacidity and neurasthenia gastrica. Whereas in diseases as- sociated with much gastric fermentation or histological changes in the mucosa that may extend to the mouth or involve it through circulatory or nervous channels, the tongue is most often affected, these diseases are gastritis, carcinoma and dilatation. In reviewing the statements of most authors on the condition of the tongue one can notice alack of clearness and precision which doubtless indicates that the relation between remote and local causes is not well understood concerning this matter. A systematic bac- - 44 — teriological and histological study of coated tongues is very much needed in association with gastric diseases. The attempt to estab- lish a definite characteristic condition of the tongue for every gas- tric disease has apparently thus far failed. The extension of glos- sitis and stomatitis to the stomach is very intelligeable by the deg- lutition of infective material. But the various forms of gastric dis- eases may also extend upwards either by eructations, or direct cel- lular continuity. Then again the oral and gastric cavities are in intimate correlation and may mutually affect each other through the vascular and complex nervous channels. Fleischer (I.e. p. 820) holds that the importance of the coating of the tongue as a sign of gastritis has been much overated, and that the tongue may be clean not withstanding very evident chronic gastritis and may be coated when this disease is absent. Nevertheless he considers the frequent coincidence of coated tougue and gastritis remarkable but attributes it to a concomitant stomatitis. General Nutrition: Chronic gastritis of long standing left untreated will inevitably affect the general nutrition. As von Noorden repeatedly empha- sized, most dyspeptics don ot eat enough and in consequence of this emaciated to such a degree that even physicians suspect a grave un- derlying disease, tuberculosis or carcinoma, where there is only a chronic gastritis. The absence of appetite is most frequently caused by suppression of secretion of hydrochloric acid. Feeling of pressure and fullness in the epigastric region is in many cases complained of and may be evident on awaking or de- velope after ingestion of food. Condition of Gastric Contents—Secretion: The results of microscopical an chemical analysis of the test meals or of lavage water early in the morning before any food has been taken, will vary according to the particular kind of chronic gastritis and according to the present state of the disease. Boas recognizes with regard to these points four varieties, viz: (1) Gas- tritis Mucosa, (2) Acida, (3) Atrophicans, (4) Anacida. l. Gastritis Mucosa or Mucipara. As was pointed out (page 97, part 1) before when Rhinitis, Laryngitis, Pharyngitis and Bron- chitis can be eliminated, then large quantities of mucus in the gas- tric contents as a rule speak for chronic gastritis mucosa. The cases — 45 — not forming much mucus are extremely rare. The mucus forma- tion can be best estimated by washing out the fasting stomach. There should be no difficulty in distinguishing between the gastric mucus and that derived from the respiratory passages. The former is generally thin, clear, glassy, stringy and flowing. The latter is thick, opaque, yellowish gray and lumpy. In the washing from the fasting organ one frequently finds organic, structural form ele- ments of the mucosa, that have been minutely described in the last chapter.' If these bits of mucosa are found at repeated washings, showing these elements either in conglomeration or singly, there can be no doubt of the existence of glandular chronic gastritis. Fre- quently the morning contents of the fasting organ show numerous leuccoytes. The contents should be drawn by expression if possible without using water. In gastritis chronica, mucipara the contents may show normal amounts of hydrochloric acid, they maybe neu- tral or alcaline. State of the Secretion: Up to recent investigations it was uniformly stated that absence or great diminution of hydrochloric acid was a constant symptom of chronic gastritis. Boas argues that there is a form of typical inflammation of the stomach termed by him. 2. Gastritis Acida in which there is a normal amount of acid or even superacidity present (Boas — Ueber Gastritis acida — Mittheil a. d. Xatur forscher versaml., Wien, 1894.). Even the mucus from the fasting stomach may turn red congo pa- per blue. In gastritis subacida or anacida the free hydrochloric acid is reduced or entirely absent, but combined hydrochloric acid may be present still. The digestion of albumen, loss of secretion of pep- sin discs or fibrin in the thermostat, is much retarded or may be wanting entirely showing the suppression of the secretion of pep- sin. Dissappearance of Rennin and its Zymogen goes on simul- taneously with that of pepsin. In cases with loss of rennin the zy- mogen of this ferment must be tested for. Atrophic Gastritis both free and combined hydrochloric acid are absent and the tests for enzymes and proenzymes are neg- ative. Milk that is taken or poured into the stomach is returned mostly in an unchanged condition. Martius and Liittke I.e., von - 46 - Noorden and others take the position that absolute deficiency of pepsin and rennet is never seen. On the basis of a large clinical ex- perience I am prepared to state that the end stages of atrophic gas- tritis give no evidence of ferments in gastric contents by any of the known tests. Nor would it be rational to suppose that hypertrophic gastritis in which the stomach is converted into a hyperplastic dense hard mass of muscle and connective tissue with no histological remnants of a glandular layer, there could be any possibility of the formation of enzymes. 4. Gastritis Anacida. In this subdivision free hydrochloric acid is diminished or entirely absent, but combined hydrochloric acid is still present. Egg albumen discs are not at all or but slowly digested in the filtrate even after hydrochloric acid. The difference between this form and the atrophic form is but one of degree as in the latter all secretion is lost completely. Age: This is preeminently a disease affecting adults, for the young are not so liable to abuse their stomachs, to be exposed to the mani- fold factors composing the etiology and their reconstructure and compensatory powers are greater. The majority of the cases are over 40 years of age. The Condition of the Bowels is most frequently one of con- stipation. The absence of the antiseptic action of hydrochloric acid favors intestinal fermentation, flatulence and metervism. The Urine is rich in urates and phosphates and gives a strong reaction for indican. The total acidity of the urine is reduced- The state of general health is a variable one, the body weight may be reduced or remain the same for years; there maybe many chan- ges of the general condition from good to bad and vice versa, but as the chronic inflammation progresses, symptoms of general dis- comfort and indisposition to bodily or mental exertion are mark- ed. Diagnosis: The determination of chronic gastritis is one of the most un- certain things in the whole domain of the clinical pathology of di- gestion. It requires careful study, not only to distinguish chronic gastritis from other diseases but to distinguish the simple, mucus and atrophic (and gastritis chronica of Boas) forms from each other. — 47 — As a rule the primary and secondary forms can be distinguished without much difficulty: Generally speaking the diagnosis of chronic gastritis can only be satisfactorily established after the pos- sibility of the existence of other affections of the stomach have been excluded. This disease may strikingly resemble the clinical picture of the gastric neuroses of ulcer and even carcinoma. As dilatation is a very rare complication, it is not a confusing factor in diagno- sis. One should not make the diagnosis definite at the first ex- amination but reserve the opinion until the patient has been studied at 3-4 visits. It has in some cases taken me much longer than that to obtain satisfactory evidence of the disease. The best evidence is obtained from repeated microscopical and chemical examination of the wash water and test meals. It will be necessary to dwell upon the differential diagnosis between chronic gastritis and the neuroses, ulcer and carcinoma. The neurosis may ' present all the symptoms of a chronic gastritis, particularly the ab- sence of hydrochloric acid, but then after patient and repeated test meal analysis it will be found that the neurosis will some day show normal and even excess of hydrochloric acid. The thing to do then is to wait for this evidence. The presence of much mucus, epithelial cells and leucocytes in the wash water from the jejune stomach, speaks for chronic gas- tritis. The demonstration of the enzymes and proenzymes is very valuable, as a normal amount of rennet zymogen and pepsinogen when hydrochloric acid is absent, (Jaworski's method of pouring in decinormal hydrochloric acid should be used.) speak for a neurosis and against gastritis. Absence of enzymes with absence of hydro- chloric acid does not easily occur in the neuroses. In the very be- ginning of chronic gastritis the enzymes may be present even in normal amount, but they disappear gradually as the disease pro- gresses. By the time the physician is consulted the enzymes are very much diminished or entirely absent, and according to Boas this is an indication of an inflammation of the mucosa and not a neurosis. The differential diagnosis between idiopathic chronic gastritis and ulcer is decided by the symptom of pain which is always present in ulcer and usually absent in gastritis chronica. -The ulcer pain is - 48 — localized, well circumscribed, very intense, and occur at definite times after taking of food. Haematemesis, of course, points to ulcer. The vomit of ulcer shows hyperacidity which is rarely present in gas- tritis. From Carcinoma the differentation is very difficult when no palpable tumor can be detected; this is intelligible when one reflects that carcinoma is always complicated with chronic gastritis. If a pyloric carcinoma is present the symptoms of stenosis, motor in- sufficiency, and stagnation of food with large amounts of lactic acid force themselves to the front. A carcinoma however seems to strike a stomach suddenly with very severe symptoms and general disturbances, pain, emaciation and vomiting, whereas chronic gastritis is characterized by slow increase of the gravity of symptoms with alternating improvements and ag- gravations. It is an important fact that the motility is not distur- bed in chronic gastritis and therefore the jejune stomach rarely contains anything but mucus and isolated cells and leucocytes. But in carcinoma the peristalsis is seriously impeded from the onset and therefore there must be stagnation, retention, and acid fermentation. These retained ingesta occur even where there is no stenosis of the pylorus, as a result of carcinomatous invasion of the muscularis. Gastrectasia is an exceedingly rare result of gastritis, it can only oc- cur from hyperplastic thickening of the pylorus, a thing seldom re- ported in the literature of this subject. As stated before presence of marked amounts of lactic acid is not observed in gastritis but in carcinoma it is frequent. Organic acids are rare in the test meals of gastritis, in carcinoma there is as a rule an excess of lactic and fatty acids early in the disease (Boas /. c). Prognosis: Chronic gastritis is a tedious but not a very serious affection, as many cases recover under suitable treatment. The prognosis must vary with the stage of the disease as presented and the intelli- gence and will power of the patient. Patients who will learn how to avoid futher detrimental influences and who have the determin- ation to carry out the dietetic and hygienic management, will recov- er. In case of incorrigible eaters or drinkers who resume tresspass- ing against their stomachs on the slightest improvement, perma- nent recovery is doubtful. — 49 - THE TREATMENT OF CHRONIC GASTRIRIS. Prophylactic Treatmnet: The prevention of the development of the disease requires avoidance of the causes given under the heading of etiology of acute and chronic gastritis. Special attention should be directed to the avoidance of continued abuse of alcohol. Every acute gastritis be it an independent, idiopathic, affection or secondary to other disea- ses must be carefully treated in order to avoid its transition into the chronic form. Very accurate directions regarding diet and mode of of life must be given to all sufferers from Liver, Lung, Heart and Kidney diseases also to diabetics in order that they may be saved from secondary gastritis, for disturbance of appetite and impairment of digestive powers must inevitably render the fundamental disease more serious. The chief predisposing factor in chronic gastritis is passive congestion, the accumulation of injurious metabolic products and heart muscle and renal insufficiency. In such cases of threatened passive engorgement, digitalis should be used early. One need not fear the appetite disturbing effect of the medicine as this is usually transient and I can confirm Leube's statement that an improvement of the appetite and of nutrition in general is observed after treat- ment by digitalis. The passive engorgement of the mucosa is more harmful than the drug. If it is noticed in several attacks that the gastric symptoms improve on digitalis it is expedient to give the remedy at the out- set of the slightest disturbance of appetite, since our experience has tought us that this will unfailingly get worse, if the stomach rebels against the remedy give the infusion by an enema into a rectum previously cleaned by warm normal salt irrigation or give it hy- podermically. Lavage: When it is no longer possible to remove the causes that led to a chronic gastritis we may yet be able to remove those that main- tain or aggravate the malady. These are the accumulation of mu- cus and the mechanical as well as chemical irritation of the stagna- ting contents, particularly when atony and hypertrophic stenosis exist. To accomplish this, emetics are unpractical because they — 50 — rarely effect a thorough cleaning and may increase the inflamma- tion by the convulsive contractions they cause and their direct irri- tation. If an emetic is absolutely not to be avoided apomorphine hypodermically is the safest. Purgatives are even more deleterious because they also increase the gastric irritation, can not be used habitually and hurry the decomposing masses into the inteslines, thereby precipitating an involvement of this tract and the danagers of intestinal putrefaction and autointoxication. Lavage is the only correct proceedurein chronic gastritis when- ever increase of mucus, absence of hydrochloric acid, decomposition and a protracted stomach digestion are evident. The mucus often adheres very tightly to the gastric walls, since it appears as a rule toward the close of the washing. Its evacuation is facilitated by allowing the water to run in under high pressure and directing'the patient to change his position, i. e. lying on his back, rising, or turning on his side during the lavage or by employing gastric mas- sage. In very troublesome lavage my double current stomach tube can be recommended (part I, page 81.). The solution-of the mucus is effectually accomplished by ad- ding 1 tablespoonful of salt and two tablespoonsful of sodium bic- arbonate or biborate to a litre of warm water. To disinfect the stomach after the removal of mucus and fermenting ingesta the following remedies are approved aids; Salicylic acid 1-000, thymol 0.5-1000. Boracic acid 10. to 1000, chloroform water 5 to 10 to 1000, shake the chloroform with the water and after settling pour off the water using only the latter. Hydrochloric acid 8.0 to 1003, resorcin sublimate 10.-1000, benzol 5.0 to 1000, solutions must be prepared only immediately before washing. The frequency of the lavage depends upon the state of the stomach; there may be cases that do not require it oftener than once in 2-3 days, others require it twice in 24 hours, as a rule once a day is sufficient. The time of the washing should be so selected that the exhausted stomach may enjoythe longest possible rest after it. For this purpose six o'clock in the evening is best adapted, as it is then about six hours after the main meal of the day and only very light diet is taken after the lavage and before bed time. In other cases this hour may be inconvenient and an early hour before breakfast must be chosen. . — 51 — Washing out the stomach is advisable only when there is much formation of mucus and where there may be stagnation of food. In atrophic or chronic gastritis without much mucus, frequent lav- age is not necessary. In these cases the stomach tube is recom- mended, not to remove fermenting ingesta or mucus, but to treat the mucosa directly, to stimulate its sluggish secretion if enzymes are still to be detected, by irrigating with decinormal solutions of hydrochloric acid; also common salt solutions are useful for this purpose (about one tablespoonful to the quart). Balneological. The use of the Alcaline Springs at Saratoga; Bethesda, Wisconsin; and those at Bedford, Pa. The waters of Carlsbad, Germany have a far famed repute in the treatment of this malady. Disinfection of the mouth should be done three times daily by wrinsing, brushing teeth and tongue with the following: R Acid Thymol ..... 0.25 Acid Benzoic......3.0 Tinct. Eucalypt......15.O Alcohol.......100.0 OI. Menth. pip...... O.75 Pour enough into giii of water to make it slightly turbid. M. If much mouth putrefaction is present, 0.8 HgCl3 Hydrag. cor- ros. bichlor. can be added, but patient must be warned not to swal- low any of the liquid. Electricity. — Both the galvanic and the faradic current should be used; the positive pole in the stomach with the Einhorn intragastric electrode, and, the broad plate electrode with the nega- tive pole should be on the cervical spinal column. — 52 — Diet.— In patients that eat very little, the appetite should first be aroused by giving the following: R Acid hydrochloric dil.....fl. siv Strychnin Sulphatis .... gr. Yi Elixir Gentian ... g. s. ad. fl. gvi Sig. M. fl. gss in §ii Aquae after meals, t. i. d. through a glass tube. In the subjoined diet list which I have suggested for my Balti- more patients, and, which is used at the private sanitarium for digestive diseases, will be found a Menu which will be more adapt- ed to the market and pallate of our American people. HEMMETER'S DIET LIST FOR CHRONIC GASTRITIS. At 7-30 A.M. . If bowels are regular, y, pint of hot normal saline solution. If bowels are constipated, a pint of cold Saratoga Vichy or plain cold water. Breakfast, 8 a.m. 100 grms. or giii^ Farina boiled with milk = 127 Calories. or 100 grms. Cerealine " " " or 100 grms. Breakfast Wheat (strained) " One soft boiled egg 80 " Two ounces wheat bread, toasted 156 . One ounce of best fresh butter 212 " One cup of wheat coffee, (made of 100 grms. of coffee made from roasted choice wheat and 150 grms. of milk). Instead of this the same portions of tea and milk or cocoa can be used = 100 cal. Sugar, 10 grms. (gii ss) 40 « The farina or cerealine will taste better if eaten with a roasted apple. As the digestive power improves, the egg is presented in form of omelette or poached, on toast. - 53 - 10.30 A.M. 100 grms. Scraped Ham (giii^) 120 Calories. 30 grms. Crackers or toast (si) 107 " 226 grms. or 8 ounces of Broth 306 " Instead of broth — milk, kefir and matzoon may be permitted in the same quantity. Dinner, 1 p.m. Soup made of 250 grms. or gviii bouillon, 30 grms. or si of rice or tapioca, 10 grms. or sii ss of butter and 1 egg = 282 cal. In case of much weakness and emaciation, Y tablespoonful of somatose should be added. The patient must not be aware of the addition of artificial foods. 120 grms. of breast meat of broiled fowl, = 288 Calories. or scraped tenderloin formed into patties and broiled, or steamed or broiled bluetish, trout, white or yellow perch, or broiled rock fish, or sweet breads. 50 grms. or gii potatoe puree = 637 calories. 100 grms. or ^iiiY carrotts, steamed 40 " or 100 grms. puree of beans or peas, or 100 grms. strained tomatoe puree, 100 grms. finely divided spinach, 1 cup custard made of 2 eggs, 160 " Or instead of this, 100 grs. of sherry gelatine, or stewed apples, or plums, or rice in form of very light rice pudding made with slices of apple, no raisins. One glass of (100 grms. - siii^) Hungarian Tokay, = 50 cal. Instead of the meats given, the patient may, for a change, be allowed broiled pigeon or venison which must not be gamy; also meat dumplings of scraped beef, scraped pork made into balls with bread crumbs, zwieback crumbs, egg and butter, cooked in bouillon and a separate sauce is made and flavored with scraped sardelles. At 3 P.M. 1 cup of chocolate made with 30 grms. or |i of breakfast cocoa or v. Mehring's Kraft Chocolade and Y pt. milk, = 135.5 Cal. 30 grms. crackers, coffee cake without grated nuts, cinnamon short cake with but the faintest trace of cinnamon, = 107 cal. - 54 — If the sweet chocolate is not agreeable, plain milk or a glass of light rhine wine with crackers are allowable. Coffee in small quantities may be added to the milk at this hour. Supper, 6.30 p.m. Broiled, panned or raw oysters, 240 grms. or gviii, = 70 cal. If there is sub or anacidity, a little grated horse raddish, lemon juice or cutsup to the raw oysters should not be forbidden. Crackers, §ii or 60 grms. = 107 calories. Butter, §i or 30 grms. =212 Yi pint of reliable rhine wine, = 50 " or Y. pint of imported beer, y2 pint of tea and milk. Instead of the oysters, — little neck clams, fresh scraped beef, finely cut roast lamb or beef, cold, smoked chipped beef or smoked tongue will answer. ULCER OF THE STOMACH. ULCUS VEXTRICULI PEPTICUM, ROTUNDUM, PERFORANS, RODEXS, COEROSIVUM, E DIGESTIONE. LCER OF THE stomach is a loss of substance of the gastric mucosa characterized by very little tendency toward healing, but rather by destructive progresssion, both in a, longitudinal direction, in a line with the internal surface as well as toward the the depth of the mucosa. It may occur in two forms; (1) the acute and (2) the chronic. The acute form extends so rapidly from the mucosa toward the peritoneum with such little lateral involvement that Rokitansky's original comparison, uAs if the ulcer were cut out with a punch," has become the classical expression of the text books. In the chronic form the destructive process is not so rapid; it extends more laterally, producing a teraced or shelving appearance of the edges and sides, so that it may be funnel shaped. Perforation into an artery vein or into the peritoneal cavity occurs in both forms. The chronic form has a tendency to healing, but in so doing causes cicatrical contractions and deformity. The acute form may terminate in healing, but owing to its limited lateral extent, the small cicatrix rarely causes deformity. u - 56 - It is very probable that the acute ulcers have a different etiology (corrosive, toxic action — trauma by sharp, hard materials in the food) from the chronic eroding type, to which the following de- scription appertains more especially. SELF DIGESTION OF THE STOMACH — GASTROMALACIA. If an animal is killed while in full digestion, the stomach may undergo self digestion providing the body is kept warm. In human beings that died suddenly, whilst the gastric digestion was at its height, it was found at the autopsy that not only the stomach had been digested, but also the spleen, and, that this process had extend- ed through the diaphragm into the lungs. The question naturally arises: What protects the stomach from autodigestion from its own secretions tinder normal conditions? This is an inquiry that concerns the fundamental properties of liv- ing matter, for it includes the non-digestion of the intestinal tract by the alcaline pancreatic juice and succus entericus, the same pro- perty as observed in the digestive tracts of invertebrates and even in the unicellular organisms, the amiebae and plasmodia of mycet- oza for instance, in whom Metschnikoff, le'Dantec, Greenwood, Saunders and myself have shown that a secretion is formed in the digestive vacuoles of the unicellular protoplasm which digests for- eign proteid material but not the living substance of the cell itself. (See—On the Role of Acid in the Digestion of Certain Rhizopods, by J. C. Hemmeter, Phil. D., etc., in The American Naturalist, Aug., 1896, p. 619). Riegel asserts that in consequence of and by means of hyper- acidity an ulcer may develope from an erosion or injury of the mucosa, which, though seemingly unimportant in itself is retarded in its healing by autodigestion. Of course it is intelligible that the hyperacidity (as Ewald, Ritter and Hirsch point out) may be the result just as well as the primary cause of ulcer. Fleischer points out that the hyperacidity may change normal clonic contractions of the gastric muscularis to intense tonic spasms that last an unnaturally long time and produce local ischaemiae and impediments to the exit of venous blood. This, if it occurs, must inevitably be followed by local disturbances in nutrition of the 57 — mucosa and eventually hemorhages of a circumscribed character, out of which the autodigestive process readily forms erosions and ulcers. ETIOLOGY. The deductions from the preceeding summary of experiments and observations are above all (the establishing of) four principal factors in the etiology of ulcer. 1. An impaired vitality or resistance of portions of the mucosa. 2. Hyperacidity or supersecretion. 3. An altered state of the blood. 4. Local bacterial infection. There are a number of well authenticated cases on record, prov- ing that direct trauma may cause gastric ulcer. (Vide Einhorn, I.e. p. 191, also others reported by C. Hoffmann, Leube and Eichhorst). According to Sidney Martin (I.e. p. 410), there are three com- mon causes of the death of the tissue which precedes ulceration. Mechanical and Chemical Causes:— Ingested fish bones, egg and oyster shells, seeds and corrosive poisions by directly destroying the tissue lead to ulceration; and an injury to the mucous membrane, which is subsequently exposed to the continued action of an irritant, will also lead to an ulcer. Interference with the Vitality of the Tissue:— The vitality of a particular part of the mucous membrane may be diminished by local and chronic disease or by interference with the circulation over a certain area. This latter usually occurs by the means of thrombosis or embolism. Thrombosis takes place in connection with disease of the vessels and in association with a di- minished quality of the blood and a slowing of the local circulation; embolism may be infective or non-infective and is usually capillary. Bacterial Infection:— The infective processes of the digestive mucosa with which we are most familiar are the ulcerative processes of typhoid fever, cer- tain dyssenteries and tuberculosis. In the gastric ulcer however there is another kind of bacterial infection, which is not accom- 58 - panied with the signs of active inflammation and is termed by some authors, bacterial necrosis. The process is characterized by the invasion of bacteria usually in the lower depths of the mucous membrane by their growth and subsequent necrosis of the tissue. Although the secretion of hydro- chloric acid is germicidal to many bacteria it must be remembered that the spores are not destroyed by it and that the invasion may take place during the periods of rest of the glands in the intervals of digestion when no hydrochloric acid or very little is secreted. There is room for the suggestion that the primary necrosis is due to bacteria and the ensueing ulceration caused by the action of the gastric juice. The bacteria can exist in the cells around and be- neath the floor of the ulcer notwithstanding a very high degree of hyperacidity. In a number of cases which I examined by the most approved cellular and bacterial stains, the bacteria were present throughout the layers even in the peritoneum, whilst the floor of the ulcer was in the muscularis. It is conceivable that they pave the way for autodigestion by causing necrobiosis of the tissues in which they are imbedded. No bacterium was so far obtained in pure culture, but the one most frequently observed was a bacillus very much resem- bling that of authrax, and the Oppler—Boas bacillus. Thermic Causes are the ingestion of very hot food and drink taken when the organ is empty. Cutaneous Burns are in some very curious causative relation to gastric and duodenal ulcers. The last two factors, hot food and large cutaneous burns explain the rather frequent occurence of gas- tric ulcer among cooks; who are in the habit of tasting foods that are still on the fire and more liable to skin burns. Constitutional Causes are generally brought about by such diseases as effect alterations and degeneration either in the compo- sition of the blood or in the vessels. These are chlorosis,anaemia syphilis, tuberculosis arteriosclerosis, fatty, amyloid and aneurys- mal degenerations of the arteries, thrombi, emboli, trichinosis and malaria. — 59 — The following table is given by Welch, representing the age in 607 cases of open ulcer collected from hospital statistics. (Pep- per's system Medicine, vol. ii). Age 1-10 | 10-20 | 20-30 | 30-40 | 40-50 1 50-60 | 60-70 | 70-80 80-90 90-100 1 over | 100 No. of Cases. 1 32 119 107 114 108 84 35 6 O 1 Totals. 33 | 226 | 222 | 119 1 7 From this table it is apparent that the largest number of cases is found between 20 and 30. Three fourths of the cases occur be- tween 20 and 60. Diagnosis:— The accompanying table shows the cardinal points in diagno- sis, of which there are really very few. The most important are haematemesis with perhaps a preceeding severe gastralgia, the chronicity of the process and the characteristic pain points i.e. the epigastric and the dorsal. The epigastric painful region is depen- dent in its limits upon the location and position of the stomach, if the latter is normal the pain point will be close to the xyphoid cartilage, but if the stomach is low down the point may be 2-3 in- ches lower. The dorsal pain area is present in about Y> of the cases (point rhachidien of Cruveilhier) and is located at about the level of the tenth or twelfth thoracic vertebra and has a lateral extent of 2-4 cm. and a vertical extension of 1-4 cm, in the majority of in- stances it is present only on the left side, though it is observed at times both on right and left and in rare cases only on the right side. A chronic process must be assumed where temporary and even quite long periods of relatively good health intervene between attacks of pain. Wherever a chronic morbid process can be determined upon with accuracy and the characteristic pain points are present at the same time, the diagnosis according to Boas should be certain {I.e. p. 41). He attributes less importance to analysis of the gastric con- tents. There are however atypical forms which present some diffi- culty in diagnosis. Thus there are cases rarely observed in which the patients never complain of pain, nor has the food any distres- sing effect upon the stomach. In other cases although pain is pres- Tabic of Differential Diagnostic Points. GASTRIC ULCER. Rare in youth, frequently increa- sing progressively from puberty to a very advanced age More frequent in women. (2:1). Quite intense, appears shortly after meals, grows severer on pres- sure; disappears at the end of the di- gesting period, sel- dom perfectly free psriods. Appetite not im- paired although patients as a rule eat less, on ac- count of their suf- fering. Dry and red, showing a white stripe in the mid- dle, or smooth and moist or slightly furred. Nothing abnor- mal. As a rule absent; if present without any bad odor. At times present frequently water brash associated with pyrosis. Appears in some cases soon aft er meals. Vomiting of a large quantity of blood, either clear red or of coffee— ground color. Blood is also found iii the stools. A repeti- tion of the haema- temesis may occur on the following day, but if once ar- rested it does not reappear for quite a long period. r. Gastric juice as a rule increased. 2. I^actic acid absent. No tu- mor, rarely how- ever if the ulcer is near the pylorus the latter becomes thickened and can be felt as a smooth lengthy body. Perforation might take place after a short peri- od of illlness. Complexion commonly fresh but anaemic after severe losses of blood. NERVOUS GASTRALGIA. Most frequent between the ages of 18 to 35. More frequent in women. The pain ap- pears without reg- ularity and is not in any way depen- dent upon the meals; is relieved by pressure and shows intervals of several days dura- tion which are per- fectly free from pain. Variable. Presents a nor- mal appearance. do. do. Not present. Shows no regu- larity in its ap- pearance. HYPER- CHLORHVDRIA. Met with iii all periods of life, ex- cept in youth, when it is quite rare. More frequent in men. The pain appears about two or three hours after meals and disappears af- ter partaking of some food espec- ially meat, milk, eggs or after the administration of bicarbonate of so- dium. Often increased, Middle age and advanced lite. No marked dif- ference between the two sexes. The pain is less intense in charac- ter but more steady; they are seldom free inter- missions during which no distress is felt in gastric region. Appetite as rule very poor. Is either clean or Almost alwaxs slightly furred. j thickly coated. do. do. Water brash and pyrosis quite fre- quent. No vomiting. No vomiting of 1 No vomiting of blood. blood. Variable. Absent. No tumor. No perforation. Complexion Pale. Increased. Absent. No tumor. No perforation. Complexion Pale. Very often bitter or sour. Asa rule present and very often associated with a disagreeable, even fetid odor. No water brash; py- rosis quite intense. The vomiting as a rule, occurs not after meals but once or twice a day or once in two days, the quantity being often very large. Vomiting of blood occurs; the quantity is re- latively small, the color ordinarily coffee brown. The blood appears in a decomposed con- dition; frequently a fetid odor. The vomiting often re- curs with short in- termissions. As a rule highly decreased. As a rule excessive Tumor very frequently pal- pable; presenting, as a rule, an un- even svirface; is painful to pres- sure and easily movable. Perforation oc- curs only in the last stages of the disease. Complexion sallow and yel- lowish; skin dry; marked cach'e- exia. - 61 — ent, it is not aggravated by taking food. In some well diagnostica- ted cases, food of all kinds was well borne. In all of these well authenticated forms, the diagnosis was assured by characteristic un- mistakable symptoms such as hematemesis and hyperacidity com- ing on afterwards. Concerning haematemesis it should be said that the differen- tiation of pulmonary from gastric hemorrhage may become neces- sary. The differentiation may be facilitated by a study of the sub- joined schema. HEA^ORRHAGE FROM Lung. Stomach. 1. Blood is bright red, foamy. {" ™°°* is dark brown, partly _ . , . coagulated — frequently mixed 2. Previous history or cardiac with fo(xL dlsease- 2. Previous history points to 3. Physical signs point to a a gastric affection or stasis in the pulmonary or cardiac affection portal system. the stomach may be affected 3. Physical examination evin- secondarily. 4. Pulmonary hemorrhage is followed by rusty colored sputa ces a gastric or hepatic affection or stasis in portal circulation. 4. Gastric hemorrhages are for days (generally) but there is ■ frequently associated with tar no blood in the stools. colored stools. The diagnosis becomes complete if the characteristic pain points are present with prompt aggravation of pain soon after taking food. Vomiting showing hyperacidity, haematemesis and a history of chronic trouble. The blood coming from the stomach does not necessarilly or- iginate from an ulcer. One may in rare instances be called upon to exclude carcinoma, portal vein stasis producing passive conges- tion, gastric varicosities, toxic corrosions, traumatisms scurvy, acute yellow atrophy of the liver. The hemorrhages of carcinoma are small in quantity compared to those of ulcer, and in cancer the blood is more frequently decomposed and of a coffee or chocolate brown color and there are rarely any bloody stools. Charcot has reported hematemesis in hysteria, [crises gastriques,] and Debove 62 — suggests (I.e.) that organic and functional nervous diseases may be coincident with ulcer. In sudden gastric hemorrhages the previous history will as a rule enable one to distinguish between the above mentioned possibilities. In hemorrhage from passive congestion due to stasis of the portal vein the epigastric pain is very slight or absent entirely. Cholelithiasis may be confounded with ulcer when there has been no blood in the vomit or stools nor any grit sand or stones in the evacuations. The following signs and symptoms are then of value. The pain in hypatic colic is not in connection with the tak- ing in of food and it draws from the median line to the right. The dorsal pain point of ulcer is located at the level of the twelfth thor- acic vertebra, to the left and very close to the body of the twelfth vertebra. But the dorsal pain point of cholelithiasis is located to the right about 2-3 fingers breadth from the twelfth dorsal or first lumbar vertebra. In ulcer there is very rarely any pain on the right side but even if there is, it is much less intense, and in chole- lithiasis there is rarely any pain to the left of the spinal colum. In cholelithiasis the right lobe of the liver is enlarged after an attack, the gall bladder also (if palpable) and during the interval between the attacks all kinds of food can be eaten with impunity. The amount of hydrochloric acid in gastric contents is normal or subnormal in ulcer-hyperacidity. Icterus when repeatedly observed following attacks of pain, strengthens the diagnosis of cholelithiasis, but it must be emphasized that with duodenal ulcer icterus is not rarely observed. In private practice I have observed a case in which cholelithiasis and gastric ulcer occured contemporaneously. Diagnosis of the Complications and Consequences of Gastric Ulcer. These are: — (1) The perforation Peritonitis, (2) Cicatricial Stenosis of the pylorus, (}) The transition of ulcer into Carcinoma or ulcus Carcinomatosum, (4) Hour glass stomach from cicatricial contractions, (5) Subphrenic Abscess, (6) Progressive pernicious Anaemia. The diagnostic signs of perforative peritonitis are, (a) great rigidity of the abdominal muscles flat abdomen, (b) Dissappearance - 63 - or diminution of Liver dullness which may be absent if only liquid gastric contents, no air escapes into peritoneum, (c) Vomiting. According to Rosenheim, (Zeitschr.f. Klin. med. b. 17, s. 116) about 5 - 6$ of gastric ulcers develope carcimata at their margins and these carcinoma are said to be associated with a pronounced hyperacidity. The socalled how glass stomach may be produced by one or more cicatrices in the neighborhood of the Antrum Pylori. Cica- trices of the duodenum may cause a dilatation beyond the pylorus thus the latter will constitute the narrowing or isthmus of what very much resembles an hour glass stomach (Reiche — Talub d. Ham- burg. Staatskrankenanstalt, 1890, p. 180). Subphrenic Abscess—Pyopneumothorax Subphrenicus. In 1880 Leyden first described a combination of diseases which followed perforative peritonitis or escape of pus from the intestines into the peritoneum. A purulent exudate forms in the lower parts of the right or left thoracic cavity under symptoms of inflammation, but no coughing or expectoration is connected therewith. The posterior and lower thoracic region gives dullness on percussion, absence of vesicular murmur and fremitus. Metallic sounds can be made out when one percusses and auscults simultaneously. The succussion sound is distinct. The lung is distinctly intact above these parts. The respiratory murmur is vescular and the fremitus maintained down to the fourth or fifth rib; from here on the respir- atory murmur suddenly ceases. The dullness that corresponds to the exudate changes with various positions of the body. The signs of equally distributed pressure in the pleura are wanting. The movements of the corresponding half of the thorax are not coordinated, the intercostal spaces almost wiped out, the heart slightly pushed to the other side. If the exudate is on the right side, the liver projects far into the abdomen and can be felt at or below the umbilicus. The exudate may perforate into the respiratory passages and cause sudden abundant expectoration of foamy pus. In 1894, Karl Madl collected 179 cases of subphrenic accumulations of pus. In 20 i of these cases, of perforating ulcers of the the stomach or duodenum were found to be the causes. Progressive pernicious anaemia as a con- comitant phenomenon of ulcer can be recognized by the reduction of the number of red corpuscles, the appearance of poikilocytes, microcytes and macrocytes. 64 - TREATMENT OF GASTRIC ULCER. Prophylactic:—If gastralgias are frequent in a person afflicted with hyperacidity, the diet must be very mild and unirritating, a milk diet will be the safest, sudden deviations in the temperature of the food must be avoided and daily evacuations must be effected by suitable diet. The dietetic and' medicinal treatment'will vary according to the presence or absence of hematemesis. (Treatment of hematemesis and the period immediately following it). During the stage of blood vomiting the patient must remain absolutely quiet in bed and not even arise for urination or defecation. Positively nothing should be permitted by the mouth not even ice. If the patient is well nourished no alimentation by the rectum is advisable because this necessarily disturbs the rest and compels the stomach to move because of the changes in position required. If the patient is weak and anaemic, a nourishing enema may be im- peratively indicated every 4 hours. The enema most favored is that of Boas consisting of 250 Gr of milk, the yolks of two eggs, a tea- spoonful of salt, one ounce of good claret and 1 tablespoonful of aleuronat flour. Previously to giving an enema for nutritive pur- poses the rectum and colon must be cleansed by a high irrigation with one liter of .warm water. The above mixture is thoroughly mixed by means of an egg beater warmed to about 99° F. and per- mitted to run in under gentle pressure, care being taken that the tube is introduced as far up into the sigmoid as possible. When the hematemesis is copious and persistent a hypodermic injection of Ergotole 20-30 minims should be given at once. With this preparation of Ergot I have had extensive experimental and clini- cal experience (see Medical News for Jan 31, Feb. 7, Mar. 7 and 14, 1891.—An experimental and clinical study of Ergot by J. C. Hem- fneter). At the same time an ice bag is placed over the epigastrium and if pain is severe an injection of Y Grain of Morphine should not be delayed as by the ease and quiet it brings about this drug acts adjuvant to the hemostatic. For three days following hematemesis this treatment should not be changed and no food allowed by mouth. The treatment from the fourth to seventh day after, consists of absolute rest in bed, a wet pack covered with oiled silk and ban- dage applied to the epigastrium. - 65 - And now one may resume feeding by the mouth but in form of liquids only. Half milk half lime water, or milk with a small addition of coffee or tea never more than lukewarm. Also Beef tea to which, lactose, meat powder or somatose have been added and egg albumen water. Chocolate, yolks of egg and all alcoholic bev- erages must be forbidden in this stage. In the second week after the hemmorrhage a typical cure for ulcer according to principles laid down by Wilson Fox, (Diseases of the Stomach, 1872, p. 146) v. Leube (Ziemssen Handbuch. vii, 2, p. 120) and v. Ziemssen ( Volkmannh Sammlung Klin. Vortr., No. 70). These systematic treatments are in the main, rest cures com- bined with the daily use of a glass of Carlsbad Miihlbrunnen water, liquid or semiliquid diet and hot applications to the epigastrium. Every morning the patient takes a glass of (40° R) warm Miihl- brunnen in which 5-10 grams of natural or artificial Carlsbad salts have been dissolved, spongiopiline cut any requisite shape and dip- ped into hot water is applied externally to epigastrium and renewed every 3 hours night and day. The diet consists mainly of milk and whipped eggs, if there is great weakness the above enemata containing perhaps §ii claret should be given, and if the pulse is feeble hypodermic injections of digitaline gr. l-30and strychnia gr. I-30. In one case of profuse haematemesis, I gave an intravenous injection of 500 c.c. of sterilized normal salt solution. The pulse had left the wrist and was barely perceptible at the carotid, the ef- fect was prompt and the opinion of the assisting colleagues was that life was saved thereby, the case recovering later on under the nitrate of silver treatment. In the third week when the pain in the epigastrium and general cardialgia have ceased, the patient may be permitted to rest on the sofa and the Carlsbad water is continued. I might remark here that the Saratoga Carlsbad acts quite as well as the imported. In fact the sole object of the Carlsbad water in the cures of Leube and Ziemssen is the neutralization of the hyperacidity and the promo- tion of intestinal evacuation. One must not gain the impression that Carlsbad waters or salts have any direct or specific curative ef- fect. Ewald (I.e. p. 275) declares that many a patient who went to Carlsbad might have recovered more rapidly if he had taken the rest cure at home. To neutralize the hyperacidity and prevent its autodigestive action. - 66 — I usually give the following:— K Magnesiae ustae Sodii Carbonatis Potassii Carbonatis a.a. 5-0 (z'\ A- Gr. xv.) Sacchar lactis 25.0 (svi f Gr. xv.) Sig. M. Half a tablespoonful dry on the tongue every 3 hours. In the third week one may permit dipped cakes, toast or zwie- back. Broiled sweet bread or calfs brain, dumplings made of finely divided meat, broiled pike, blue fish, trout, oysters in very small quantities. In the fourth week purees made of potatoes peas or beans, rubbed through a sieve, stewed apples, pears and plums. A glass of approved claret mixed with Saratoga, vichy may be allowed. All vegetables that can be made into puree (gruel) from such as spinach, carrots, peas, etc., etc. For many years the patient must avoid raw fruits, all sour, acid or spiced food and drink, ice cream and all cold and hot beverages. If there has been no haematemesis the treatment had best be carried out along these lines also. In re- bellious cases of recurrent gastralgias, vomiting and hyperacidity, McCall, Anderson (Brit. Med. Journal, 1890, May 10) and H. B. Donkin (the Lancet, 1890, Sep. 27) recommend a total abstinence cure of 2 to 3 weeks, during which the patients are fed exclusively by rec- tal enemata (3 to 4 in the day). Hot applications to epigastrium are also used. After 10 days of rectal feeding they cautiously and slowly return to feeding by the mouth (milk buillon, egg albumen). I have tried this in a number of cases in whom relapses had occured after the rest cure and can speak in favor of the method. Ger- hardt and Boas speak very favorably of nitrate of silver in light cases of gastric ulcer. The latter begins with R Argenti Nitratis 0.25 to 120, pepermint water—one tablespoonful 3 times a day on an empty stomach—then the dose is increased toO.3 to 120 of wa- ter of which two bottles are taken and finally 0.4 to 120 water of which also two bottles are advised. This is combined with a spar- ring diet and as much rest as possible. Fleiner and Kussmaul recommend Bismuth subnitrate in all irritative conditions of the gastric mucosa—old ulcers, erosions, ex- coriating carcinomata. Fleiner employs it in the following man- ner;—10 to 20 grams (150 to 300 grains) of Bismuth subnitrate are - 67 - stirred in 200 c.c. of warm water. After the stomach has been thoroughly cleansed by lavage, this suspension is poured into the stomach and allowed to remain 3 minutes, then the clear water is siphoned, out the Bismuth remaining behind and forming a coating to the injured places in the stomach — it is a modified direct or lo- cal treatment. I usually employ five drachms of Bismuth subnit- rate and one drachm of Bismuth subgallate in a pint of warm wa- ter—having previously thoroughly cleansed the stomach with so- lutions of sodium bicarbonate (gss to pint). In cases in which Fleiner's treatment can be employed it relieves pain promptly, re- duces the hyperacidity and promotes healing, it is worth trying. The anaemia following ulcer may require iron arsenic, strychnin. Iron preparations must contain no acid. Surgical Treatment becomes necessary when after a trial of aforesaid methods the ulcer or ulcers prove very obstinate and not amenable to medical treatment because hemorrhage may be- come so abundant and frequent as to endanger life, or lastly, be- cause of perforation. Nelson C. Dobson, (Bristol Medical Surg. Jour I. I883) first advocated surgical interference for perforating gastric ulcer. In this country Robert F Weir of New York has con- tributed the most important work to this domain of surgery. His last important paper (Rob. F. Weir and E. M. Foote—The Surgical Treatment of round ulcer of the stomach and its sequelae, etc., Medical News, April 25 and May 2, '96) contains.an account of seventy-two cases of laparotomy for acute perforation of gas- tric ulcer. For particulars concerning the surgical treatment of gastric ulcer the«reader is referred to textbooks on abdominal surgery and the publications of Weir. Gastric ulcers have recently been ec- cised entirely, the sequelae thereof have been removed by severing of peritonitic adhesions and hour glass stomach much improved by gastro anastomosis (see v. Hacker — Ueber Magenoperationen bei carcinom u. b. narbigen stenosen, published by Wilh. Braumtiller— Wien and Leipzig 1895)- CARCINOMA VENTRICULI. CANCER OF the STOMACH. QASTRIC CANCER is characterised by the progressive cach- exia which distinguishes it from all other chronic affections of the stomach. It is not sufficient for diagnosis and therapy to diagnose the simple presence of cancer, since these neoplasms vary so greatly; according to their location at the cardia, the curvatures and the pylorus and in so many important symptomatic and diagnostic points, that they compel separate consideration. It is expedient to consider these malignant tumors under three headings, vid:— (1) Carcinoma of the cardia, (2) of the body of the stomach, i. e. the curvatures and the fundus and walls, (3) of the pylorus. Carcinoma of the Cardia: — (a) Signs and symptoms, complaints of an uncomfortable feeling of a foreign body and of pressure above the gastric region, particulary after the ingestion of food. Sensations of pain are not contemporaneous with swallowing of food but occur independantly. On ingestion of food a sensa- tion as if the same becomes clogged or is caught before it reaches the stomach; patients imagine that copious draughts of water gives relief, most likely because this can pass through the stenosis caused by the neoplasm. Another important symptom is vomiting, which is not actual gastric vomit, but the wretching up of mucus and few food particles. The cause of these regurgitations of masses of mu - 69 - cus is the formation of a large dilatation of the oesophagus above the stenotic cardia carcinoma. In this oesophageal diverticulum or dilatation, the food is caught, retained, putrefies and is eventually vomited up again. There is also a catarrhal oesophagitis present at this place. Liquid or semi-liquid substances may for a long time be able to pass, while relatively solid substances give rise to the difficulties stated. Later on, as the stenosis increases, liquids can not pass either, and loss of appetite and strength goes on uninterrupt- edly. If an obstacle to the passage of the sound can be ascertained at the entrance to the stomach in a person over 30 years of age the diagnosis of cancer of the cardia becomes certain. Under all such suspected cases only a soft elastic tube should be used for explor- ative sounding. In two cases in private practice during the last three years I was enabled to establish the diagnosis by microsco- pical examination of small portions of the carcinoma that were brought up with the sound. These neoplastic fragments are occa- sionally found in the eye of a lower opening of the sound and they constitute a definite criterion. In one of the above cases, the diag- nosis was confirmed by my colleague Dr. Einhorn and in the other by autopsy. In addition to the sounding and the cancerous frag- ments the following signs are of diagnostic importance:— 1. Percussion of the region over xiphoid cartilage is very pain- ful. 2. On the sound blood will frequently be found mixed with the extremely foetid mucus, and at times nests of cancer cells. 3. On placing a stethoscope over the epigastrium, normally two deglutition sounds can be heard. One is synchronous with the beginning of the act of swallowing and the other is heard from seven to twelve seconds later. Now in carcinoma of the cardia, the second deglutition sound which signifies the entrance of liquid into the stomach may be much delayed or absent entirely, this sign is of importance per se. 4. Supraclavicular swelling of the lymph glands, if palpable, support the diagnosis also. 5. Lauenstein asserts that there is a systolic murmur audible in the epigastrium, due to pressure of the tumor upon the aorta. According to Boas this is an inconstant sign. — 70 — Duration of the disease is 6 to 9 months after the first symp- toms are manifested, death occurs as a result of gradual exhaustion, marasmus, aspiration pneumonia, secondary carcinomata in the liver and other organs and intercurrent hemorrhages. Differential diagnosis from chronic gastritis is difficult in the beginning of the cancer, as in both the presence or absence of hydrochloric acid is no criterion, but as the cancer progresses, the sound will settle the doubt in locating the stenosis. From oesopha- geal ulcer, the cardia carcinoma is differentiated by the fact that pain is immediately associated with deglutition of food, by the age of patient, (see tables of ages at which ulcer and cancer are most fre- quent) by the haematemesis and the bloody stools of ulcer. Ulcer of the oesophagus is extremely rare in comparison to cancer. From diverticulum, the cardia carcinoma is differentiated by the following facts.— Diverticulum is frequent in the upper third, rare in the lower third of the oesophagus. The permeability of the gullet will more variable than in cancer, because the sound will of- ten skip the diverticulum. In the latter there will rarely be pain and the marasmus will not be so progressive and rapid. From Cardiospasms or cramp of the cardia, the carcinoma is differentia- ted by the occasional free passage of the thickest tubes in the for- mer, which occurs only in neurasthenics. Nutrition is not so much damaged as in cancer. If tuberculosis or syphilis is present, one must think of the pos- sibility of the neoplasm being caused by these diseases. Treatment of Cardia Carcinoma:— As long as there is no cure possible, this must be palliative. During the time that deglutition still brings liquid food into to stom- ach, the sufferer must be carefully fed on highly nutritious liquid diet. Liquid eggs and wine as described in the diet of gastritis, beef tea, soups of fluid potatoe or pea puree in bouillon, Leube-Ro- senthal beef solution, v. Mehrings Kraft chocolate, Egg nogg. When pain was great I have found that chloral hydrate gr. xv. t.i.d not only relieved it but acted as a local disinfectant in the diverti- culum above the stenosis. Boas recommends iodide of potassium in doses of 15 grams 3 times daily as aiding in keeping the oesopha- gus from closing up as soon as it would otherwise. Arsenic is said to effect the same prolonged permeability. — 71 — In one case I succeeded in keeping the oesophagus open for six month by intubaling with an inelastic tube 4 in. long and as wide as an ordinary Ewald tube. The tube was removed every 10 days and replaced. Patient lost no weight in those six months, but even gained. Death was caused by aspiration pneumonia during a per- iod in which the tube was left out in order to rest the oesophagus from the stout cord with which the tube was connected whh the mouth and was usually tied around patient's neck. When deglutition is impossible the only thing left to be done is gastrostomy. If the patient can be persuaded to undergo this operation, it should be done before marasmus proceeds too far, as it then prolongs life much more and the shock of the operation is stood better. This operation consists in making an opening into the stomach for purposes of feeding the patient by passing food directly into the organ. F. Kaiser (in Czerny Beitr. z. operativ. chirurg.) collected 31 gastrostomies, of these 28 died of the immediate results of the op- eration. Zesas (Archiv f. Klin. Chirurg. bd. 32, S. 188) reported 131 cases from literature, mostly oesophagus cancers which in their stenosing effects are identical with those of the cardia; among these only 19-5$ recovered from the operation sufficiently to call this a success, because real cure is out of the question, it is a palliative measure only. CARCINOMA OF THE BODY OF the STOMACH. Cancer of the Fundus, Anterior or Posterior Walls and the Curvatures. Subjective Signs:— 1. Sudden abrupt beginning of the disease, striking an appar- ently healthy organ. 2. Loss of appetite in 90$ of cases. 3. Aversion to meat. 4. In stenosing pyloric cancer there is much thirst. 5. Frequent eructations which, when there is dilatation can be very offensive. 6. Pressure in the beginning, pain later on. — 72 — 7. There is frequently vomiting which is more copious in pyloric cancers because of the accumulations from the dilata- tion. Frequently the vomit has a coffee ground appearance and the haemin test (refered to in part 1.) proves the presence of blood. The state of the bowels is variable. The vomit contains as a rule no hydrochloric acid, but excess of lactic acid. Objective Signs:— On Inspection, Palpation and Percussion a tumor can be made out in at least 50$ of the cases. Tumors of the pylorus do not move with the respiratory move- ments unless attached to the liver; tumors of the curvatures generally show distinct respiratory movements. Examination of Stomach contents:— The results will be characteristic in most cases and evince. 1. Grave interference with the motility. 2. Suppression of secretion. 3. Products of stagnation dependent upon these. The distur- bances of peristalsis are due most likely to a direct invasion of the muscularis by cancerous proliferation. The simplest way of testing the motor disturbance is to cleanse the stomach thoroughly by lav- age in the evening, giving a test supper thereafter and examining the following morning when normally the stomach should be empty but in carcinoma much food and mucus with absence of hydro- chloric acid and presence of lactic acid will in 88$ of the cases*be found. Hydrochloric acid is absent in 88$ of the cases, in carci- nomata that have arisen from old ulcers, there is claimed to be a secretion of hydrochloric acid until the last stages of the diseases. This assertion of Rosenheim's is not always correct as we have shown twice this winter at our clinic. If the glandular layer is in- vaded, secretion must cease no matter whether the carcinoma arose from an ulcer or not. Lactic acid is tested by Uffelmann's reaction, in carcinoma there is an excess in from 86 to 90$. Demonstration of the long, base ball bat shaped, Oppler—Boas bacilli is according to Kaufman, Schlesinger and Riegel, a very important sign. There Should always be a careful lookout for histological evidences, bits - 73 - of the growth in the wash water and vomit, this clinches the diag- nosis. Secondary symptoms are anaemia and cachexia oedema of the an- kles in 15 to 20$ of the cases. The urine contains excess of nitrogen excretion, indican and pepton. Latent cancers may occur, they are very rarely observed however at the autopsy. Ulcus Carcinomatosum:— The diagnosis is made from a history of ulcer, years of gastric pain, not a sudden abrupt beginning and presence of hydrochloric acid even hyperacidity — Haematemesis and blood in the stools in the previous history points to origin of the carcinoma from ulcer. Simple uncomplicated ulcer may cause a tumor-like thickening, simulating cancer; here the analysis of contents may even show ex- cess of lactic acid owing to motor insufficiency and cicatricial sten- osis and the diagnosis then becomes difficult. As is also the dif- ferential diagnosis of ulcus carcinomatosum from simple hyper- trophic stenosis of pylorus, fortunately such states without any other important signs are rare. Treatment:— There is no successful medicinal treatment for this disease. Life may be most prolonged by a suitable diet, as nutritious as pos- sible and adapted to the individual. A highly nutritious proteid carbohydrate and fatty diet should not be interdicted as long as the motility is good and the patient's strength can be upheld by intesti- nal digestion. Where there is stagnation owing to pyloric obstruc- tion, the carbohydrates and fats must be diminished. The best tonic for the stomach is daily lavage, even where there is not much stag- nation, but where the latter is marked and accompanied by fermen- tation, antiseptics must be added, such as boracic acid, 20 to 30 to 1000 H20, salicylic acid 3 to 1000 H20, sodium benzoate 10 to 30 to 1000 H20, Resorcin 10 to 30 to 1000 H20, Thymol 5 to 1000 H20, Lysol 1 to 2 to 1000 H20. Hydrochloric acid 4 to 5 to 1000 cc.H20. It is always well to get the stomach clean by using nothing but warm salt solution and finishing the lavage by the last irrigation with one of the disinfectants of which I prefer hydrochloric acid. A tonic which has been serviceable in my experience and will — 74 — arouse appetite and promote digestion in the invaded organ, if this is at all possible, is the following; K Extract Condurango, fl. gxii. Strychnin Sulphatis, gr. Yi. Hydrochloric Acid dil., gr. Y>. Elixir. Gentianae, g. s. fl. gvi. Sig. M. Take §ss. in §ii aquae after meals through a tube. When there is much anaemia, the following formula has my preference in this disease as well as ulcer; Solution of Iron and manganese, (Parke, Davis d Co.) fl. gvi. Liquor Potassii arsenit min. xlviii Misce. fl. §ss. t.i.d. Constipation is best met by large colon irrigations, Cascara Segrada, fl. Ext. or Syr. Activ. (Clinton Pharmac. Co.). Diarrhoea must be met by Salol, Bismuth Salicylate, or Ben- zonaphthol. Opiates are not advisable for this symptom. For pain, hot external cataplasms and 20 to 30 drops of comp. spir. of ether should be first tried. If severe, codein, gr. Y extract. Belladonnae, gr. Y in §i. pepermint water generally relieves it and may be repeated if requisite. The pain is rarely so intense as to require hypodermic injections of morphine. Lavage systematically and scientifically employed seems to prevent pain, it certainly pro- longs life and sometimes apparently works wonders for these pa- tients. DIET FOR GASTRIC CARCINOMA. At 8 A.M. 100 gr. milk with tea (67.5 + 50 gr.) = 174. cal. toast + 10 gr. butter = 336.6. cal. At 10 A.M. 100 gr. fried or broiled perch, pike or trout = 72. Calories- 50 gr. toast = 129. " Instead of this calfs brain, sweet bread or 2 eggs are recomen- ded for change. - 75 — At 12 M. 150 gr. milk rice = 260. Calories. 100 gr. breast meat of fowl = 142.45 « 50 gr. maccaroni =126 " 200 gr. finest claret =100 " When motility is good, mashed potatoes and puree of peas or beans are permissible. At 3 P.M. 100 gr. tea with milk + 50 gr. cakes = 254 Calories. At 7 p.m. 100 gr. cream =214.6 Calories. 50 gr. toast + 10 gr. butter -f 30 gr. scraped raw beef or ham = 376.3 " At 9 P.M. 50 gr. rich milk or a glass of tokay, a few crackers, chocolate is permissable, young pigeon, partridge and prairy chicken also. If the motility is good one must not be too severe on the patient's de- sires for food, many cases can live and gain strength on a ordinary nourishing diet when it is not retained too long in the stomach; un- der these circumstances, mutton chops and beefsteak broiled after they are finely minced may be allowed. Surgical Treatment:— As already mentioned, gastrostomy is a palliative operation for malignant tumor of the cardia and oesophagus, to permit of direct introduction of food by establishing an opening between the stom- ach and the abdominal wall. In carcinoma of the pylorus, another palliative operation is practiced, where it is impossible or inexpedient to remove the growth, under the name of gastroenterostomy. This consists in the establishment of anew communication between the stomach and the small intestines, thus allowing the chyme to reach the intestines without passing the pylorus. The radical operations are resections of the pylorus and excision of the tumor no matter where it may be situated in the stomach. These operations are contraindicated if metastases are detecable in other organs, by the presence of great anaemia or cachexia, large size of the tumor—adhesions to other organs. The detailed descrip- - 76 - tions of these operations belongs to text books on abdominal sur- gery;— See surgery of the alimentary canal, by A. Ernest Maylard, P. Blakiston, Son and Co., Phila., 1896. Abdominal surgery by J Geieg Smith, published by P. Blak - iston, Son and Co., Phila., 1896. Surgery by American authors, by Roswell Park, vol. ii, chap. 8, published by Lea Bros., Phila. System of surgery, by Fred S. Dennis, vol. iv, p. 217- Abdominal surgery, by M. II. Richardson and Farrar Cobb. A Text book of abdominal surgery, by Skene and G. S. Keith. FredJk Treve's Manual of operat. surgery, vol. ii, p. 405. Franz Koznig, Lehrbuch d. speziel. chirurg., bd. ii, s. 281. Penzoldt and Stintzing's Handbuch d. speciel. therapie,. vol. iv, p. 444. The operative treatment of gastric disorders, by Prof, von Heinecke. Erlangen. The following table gives the age in 2038 cases of gastric can- cer, obtained from trustworthy sources and arranged according to decades: (By William H. Welch, I.e.). AgC | 10-20 | 20-30 | 30-40 | 40-50 | 50-60 | 60-70 | 70-80 | 80-90 | 90-100 over 100 No. of Cases. 2 55 271 499 620 428 140 20 2 1 Percent. | 0.1 | 2.7 | 13.3 | 24.5 1 30.4 | 21 | G.85 | 1 | 0.1 | 0.05 From this analysis we may conclude that three fourths of all gastric cancers occur between forty and seventy years. The abso- lutely largest number is found between fifty and sixty years, but, taking into consideration the number of those living, the liability to gastric cancer is as great between sixty and seventy years. Nevertheless the number of cases between thirty and forty years is considerable, and the occurrence of gastric cancer even between twenty and thirty is not so exceptional as is often represented, and is by no means to be ignored. The liability to gastric cancer seems to lessen after seventy years of age, but here the number of cases and the number of those living are so small that it is hazardous to draw positive conclusions. — 77 — Morbid Anatomy:— The following table gives the situation of the tumor in 1300 cases of cancer of the stomach: (From article by Wm. H. Welch, I.e.). Pyloric Region. Lesser curvature j Posterior Cardia. Wall. Whole or greater part of Stomach. Multiple Tumors Greater curvature Anterior Wall. Fundus. 791 60.8$ 148 11.4$ 104 68 8$ , 5-2$ 61 4.7$ 45 3-5$ 34 2.6$ 30 2.3$ 19 1.5$ From this table it appears that three fifths of all gastric can- cers occupy the pyloric region, but it is not to be understood that in all of these cases the pylorus itself is involved. In four fifths of the cases the comparatively small segment of the stomach represen- ted by the cardia, the lesser curvature, and the pyloric region is the part affected by gastric cancer. The lesser curvature and the an- terior and the posterior walls are involved more frequently than appears from the table, in as much as many cancers assigned to the pyloric region, extends to these parts. The fundus is the least fre- quent seat of cancer. In the cases classified as involving the grea- ter part of the stomach the fundus often escapes. GASTRECTASIA. MOTOR INSUFFICIENCY. DILATATION OF THE STOMACH. BOAS RECOGNIZES a mechanical insufficiency of the first degree (Mechanische Insufficienz ersten Grades) which is a myas- thenia or atony of the gastric muscularis in which the ingesta remains in the stomach too long but finally are completly moved out into the intestines. There is no absolute retention of food but simply a delay in the expulsion. The fully developed dilatation Boas calls mechanical insufficiency of the second degree. Riegel differentiates: — 1. Simple Atony or Insufficiency of the stomach. 2. Atonic or typical ectasia or dilatation. 3. Secondary ectasia or pyloric stenosis with ectasia. Naunyn speaks simply of motor insufficiency and Rosenbach of mechanical stomach insufficiency. Schreiber, (Boas — Archiv f. Verdauungs krankheiten, bd. ii, p. 423) in attempting to select a designation which shall signify the most constantly present condi- tion of all these morbid states of motility and one which shall unite them all around itself, reached and suggested the terms Stasis stomach (Stauungs-magen) with permanent digestion or permanently diges- ting stomach. Besides being a cumbersome circumlocution, the term does not even include all conditions of this type, for in Boas' mechanical insufficiency of the first degree and in Riegel's simple — 79 — Atony— conditions which I am convinced really do exist, there is certainly no permanent digestion. Permanent digestion goes on in fully developed dilatations with impaired peristalsis as long as hydrochloric acid and ferments are secreted. But as there undoubtedly are long standing dilata- tions with complete achylia gastrica or loss of secretion, (Einhorn) there can be no digestion in them. The fact that the food is over- retained in them does not imply that it is digested, only in dilata- tions that show hydrochloric acid and ferments, can we speak of permanent digestion. The efforts of Schreiber to establish Reich- mann's chronic secretion as a complication of dilatation with retained food products and permanent secretion caused by stimulation of the retained food are very convincing-we shall speak of the patho- genesis of gastrosuccorrhoea or Reichmann's disease under the ner- vous affections of the stomach. It is impossible however to invent a term which shall comprise the important features of all types of motor and mechanical insufficiency and probably as clear a classi- fication as any is one based on Riegel and Boas. 1. Simple gastric atony or motor insufficiency or myasthemia without dilatation. 2. Atonic dilatation—motor insufficiency due to relaxation of the gastric walls, without pyloric stenosis. 3. Secondary dilatation due to pyloric stenosis. It it self evident that these conditions may have widely differ- ent causes, but the one common sign is not the retention of food nor permanent digestion, but the impaired motility. Etiology:— Two kinds of cases may occur: either the atony of the gastric wall is not due to a mechanical obstacle; in this case nothing will oppose the free course of the contents, and they will only linger in the stomach because the latter is really incapable of ejecting them from its cavity in proper time, or the atony will be due to a pyloric stenosis; the muscular tonicity will have been overcome by an im- passable obstacle, the fibres exhaust themselves in contending with a too strong resistance, and the dilatation may then be considered as following on existence of the obstacle. In the first case, the etiology is variable, and arises finally from a difficulty in the nutrition of the wall; in the other case it is purely mechanical. — 80 — Dilatation Through a Mechanical Obstacle:— The causes capable of opposing the passage of stomach con- tents into the intestine, and of opposing such a resistance to the contractions of the stomach that it dilates, are first of all the constric- tions of the pylorus. These are generally the result of an anatom- ical alteration; cancer or cicatrices of circular ulcer, in the ma- jority of cases, determine the constriction of the pyloric ring. To these causes mnst be added a proliferation of the muscular fibres and of the tissue adjoining this ring, a veritable tumor, benign in character, but the mechanical effects of which are practically ana- logous to those of the ulcer and of the cancer. Nauwerk was one of the first to draw attention to these facts. A spasm of the pylo- rus, which can be compared to a spasm of the spinchter of the anus, can just as well determine an occlusion of this orifice. This spasm, which has been admitted by authors, for a long time, for reasons a little theoretical perhaps, has been demonstrated since gastric sur- gery has permitted the more direct exploration of this organ. Mar- tin, among others, has seen a pylorus, large enough to admit the passage of two fingers, bring on a considerable dilatation by its spasmodic occlusion consequent upon a circular ulcer after which had occured a considerable hyperacidity. Lastly, just as there is said to exist a pure mitral constriction of congenital origin, so Lan- dour is said to have proved the existence of a pure pyloric constric- tion. He is said to have collected ten observations, and to have shown that this orifice, large enough during infancy, might under- go an arrest of development and remain very small, while the stom- ach grows larger with age, a serious dilatation would result from this conjunction of circumstances. However, the obstacle need not necessarily have its seat in the tissue of the pylorus itself. We have elsewhere said that a polypus inserted in the gastric cavity was capable of bringing about a dila- tation by becoming fized more or less in the intestinal orifice, and thus causing its occlusion. Deiters has collected at the anatomical- pathological instituie of Greifswald a somewhat large number of observations in which congenital malformations, abnormal foldings, diverticulae, and atresia had provoked dilatations by constricting the intestine in the more or less immediate vicinity of the pylorus. An anatomical lesion of the duodenum, the cicatrix of an ulcer, for — 81 — example, would produce the same effects by diminishing the calibre of the passage. There exists also a whole series of obstacles of extrinsic origin., which by compression of the pylorus or of the under-lying portion of the intestine, have a tendency to bring about the same conse- quences as the causes hitherto mentioned. There are, firstly; peritoneal adhesions, circumscribed or not, the results of former inflammations. The cicatrix of a circular ul- cer may be placed in such a way that it may not be able to hinder directly the course of the chyme over its own location, but the fib- rous tracts which radiate from its basis as a rule contract more every day, and end by obliterating the lumen either directly, or by mak- ing the under-lying intestine describe an abnormal curve. The liver and the pancreas are equally, (in some cases) the start- ing-point of inflammations which will leave in their train, similar anatomical modifications. The head of the pancreas, so intimately connected with the duodenum, may become cystic or cancerous, and cause by compression a duodenal stenosis with following dila- tation of the stomach. A congenital displacement of the same or- gan would bring about the same disorders. (Cechini). A biliary concretion, by dilating the ampulla of Vater, or by compressing the intestinal wall, may produce a compression of the duodenum suffi- cient to bring about gastric dilatation; Grundzach has recently re- ported a case of this kind. Bartels, Mueller, Warnek, Litten and other authors have studied the relations of ectopy of the right kid- ney and of gastric dilatation. These studies have been continued in an interesting work by Bruhl, and Mathieu has also just recently reported new cases (Societe Medical d' Hospitaux). The persons presenting this coincidence of movable kidney and dilatation of the stomach, are usually young girls or women of the working class, who are in the habit of fixing their skirts at the level of their hips with laces very tightly drawn, causing an external constriction, which is shown by the presence of a permanent furrow. In other cases, men, who wear a belt or strap, produce the same results. The right kidney thus becomes displaced forwards and inwards, pressing upon the fixed, descending portion of the duodenum, which is situated between the hilum of the kidney and the vertebral colum. Such partial obliteration of the intestine would bring about a slower — 82 — and more difficult evacuation of the contents of the stomach. As food would remain longer in the stomach, there would result first an in- crease of activity and a slight hypertrophy, then later, a muscular relaxation, a distention of the walls and a dilatation of the cavity of the organ. Ewald and Pertick have gathered together a certain number of cases in which a hernia of the floating portion of the duodenum, or of the first part of the jejunum across a laceration of the mesentery, or a diverticulum of these parts of the intestine, has played the same part, and caused in the end a gastric stasis. Dilatation Without Mechanical Causes:— Besides the cases in which mechanical obstruction causes a dil- atation, one sees gastric atony follow upon a whole series of gene- ral affections. Weakness of the walls is in these the only cause which can be supposed, and these cases constitute the second group of which we spoke at the beginning. Dilatations of this class which seem to be primary, may be acute or chronic. The first kind have for their cause either a trau- matism, or a surgical intervention (laparotomy,) or else a serious injectious disease; Bartels, Hilton Fagge, Lepoil and Montaya have cited examples in which typhoid fever seems to have played the part of the chief cause. In this case generally, the dilatation seems due to the loss of tonicity of the musculature of the stomach and of the abdomen. In other cases, the origin of the evil is an excess of food, an error comitted so frequently by convalescents confined to one diet for a long time. Chronic dilatations are dependent upon a great number of fac- tors. First of all, large eaters suffer first with distention of the stom- ach, then later with dilatation; this phenomen is comparatively fre- quent with persons into whose ordinary diet enters a large quantity of liquids: such is the case with excessive drinkers of beer, which acts not only mechanically by its volume, but also through the ir- ritating and poisonous substances with which it may be adulterated. The milk treatment might just as well, when ill administered, bring about a distension, and later a dilatation of the stomach by a su- perabundance of liquid food; Debove has especially drawn attention to the drawbacks, of prescribing milk in considerable quantities, and 83 - has cited, among others, a case of circular ulcer cured by the daily allowance of eight litres of milk; but an enormous dilatation of . the stomach resulted. In a general way, it must be admitted that over-feeding produces a certain amount of inflammation. The dilatation is produced under this double influence of the catarrh and of the distention; without the addition of the first of these causes, megalogastria alone would occur. We have seen that chronic catarrh or simple chronic gastritis can have as its consequence a considerable atrophy of the muscu- lar fibres of the stomach, and that an enormous dilatation of the stomach is sometimes the result. The same may be said of dy- spepsia, provided that it is one of the forms where a hyperacid secre- tion causes a prolonged stasis of the amylaceous substances; such cases have been collected by Mathieu and Remond, under the name of dyspepsia with organic hyperacidity and stasis, In other cases muscular atony is the result of a prolonged stay in the stomach of undigested food, with fermentation thereof, when hydrochloric acid is wanting. Drawn out by a weight more or less considerable, and distended by the gases that are developed in the putrefying mass, the muscular fibres lose the faculty of withdrawing back upon them- selves. Futhermore, since the glands become diseased, and since the inflammation is not limited, as we have shown, to the glandular tunic alone, but on the contrary invades to a variable degree, it is true the body of the wall, one must not be surprised to see the atony very soon become difficult to cure. The dilatation found in con- sumptives, in chlorosis, etc., is caused solely by chronic gastritis, which is caused by blood alterations, the results of these diseases. In diabetes, both the chronic gastritis and superabundance of food, take part in the alteration of the walls and may finally lead to amyloid and colloid degenerations of the muscular fibres. Atony which is purely nervous, concerning which Germain, see and Mathieu have published numerous researches, is produced in consequence of crises appearing to indicate the successive and al- ternating intervention of a particular state of spasm, and of atony of thegastro-intestinal system. These crises are produced by an occasional and general cause such as sad emotions, mental shock, etc. Neurasthenia then takes part in the etiology of dilatation, in the same way in which we have seen it become one of the import- -84 - ant factors in syndrome dyspepsia. The atony due to neurasthenia can be just as well brought about by lesion of the central or peri- pheral nervous system, and the dilatation will then depend on a deep seated alteration either of the centres, or of the peripheral nerves. Glenard has represented general ptosis of the abdominal organs, as the expression of a particular diathesis, a condition of relaxation of the tissues with smooth muscular fibres, and has con- sidered the dilatation as depending upon this general state. Al- though we have not verified the lesiens upon which Glenard has built this theory, we cannot deny the existence in clinical medicine of cases analogous to those described by this author; such are the dilatations through nephroptosis. Pathological anatomy:— If the etiology of dilatation is complex, its pathological anatomy is simple, and to a slightly variable degree, the lesion is always the same. At the autopsy of a subject dead from cancer of the pylo- rus, for instance, one finds the abdomen filled by a voluminous sac which comes down more or less near the ptibes. This sac, which represents the stomach having lost all its normal relations, and ex- cessively dilated, may contain enormous quantities of liquid, and the ancient authors who knew only the extreme cases, have cited extraordinary examples of this. Plempius is said to have seen a stomach that held nine pints of liquid; Stengel mentions a stomach containing twelve "measures"; Schurig, a stomach containing forty-eight litres; Henricus ab Herr found a stomach which filled the whole of the abdomen. The walls of this gastric sac have become thin; in general, this thinness is found in all the coats, and with the microscope one finds an atrophy of the mucosa; at the same time, the submucosa is now composed only of isolated bunches of muscular fibres separated by the connective tissue. When the dilatation is caused by an ob- stacle at the pylorus, hypertrophy of the muscular wall is produced first; then a veritable interstitial sclerosis comes on little by little submerging the true elements, and the atony of the wall is due to ' the disappearance of the contractile fibres; an apparent hypertrophy through exaggerated proliferation of the connective tissue, some- times masks in these cases the actual atrophy. The muscular hy- -85 - pertrophy continues very long in the pyloric region where it also attains its maximum point, and we have seen, while studying the ulcer, the increase of resistance and of the volume of the walls, which sometimes results, may simulate a tumor. A stomach which has undergone acute dilatation may present veritable linear thickenings of the serous coat. This modification precedes the rupture of the organ, the symptoms of which we shall have occasion to describe further on. The anatomical-pathological study of a dilated stomach in- cludes naturallv that of the causes of the dilatation which we have already described. A dilated stomach may present variable forms due to the action of a special cause. If a cicatrical or scirrhous constriction causes the cardia and the pylorus to approach each other, the stomach will be pyriform; but if the same lesion has ploughed a furrow, more or less deep, on the wall, a dilatation in the shape of an hour-glass will be produced. But these are anato- mical curiosities, and the symptoms do not differ from those caused by occlusion of the pylorus. SYMPTOMS. State of the Appetite:— The symptoms of dilatation are very variable. The appetite may have completely disappeared, or have become considerably de- creased, some patients, for instance, will not need more than one meal a day. In other cases, since the stomach merely plays the part of a reservoir with no outlet, and the foods being no longer evacuated from the stomach into the intestine, digestion and ab- sorption occur no longer; the patients may be tormented with hun- ger, and they are in an analogous situation, as far as effects are con- cerned, to that of persons seized with an impassable stenosis of the oesophagus. They try then to satisfy their appetite, and yielding to the solicitation of hunger, present veritable bulimic phenomena. In reality, it is not hard to understand this difference which depends, practically, on the nature of the obstacle to the course of the foods; anorexia is observed chiefly in cancerous patients and those seized with chronic gastritis; while a cicatrix of a circular ulcer may have obliterated the pylorus without bringing about very clear modifica- tions of the special-sensibility of the stomach. - 86 — Pain:— Pain is not usually very acute; it consists rather of a sensation of fullness and of tension, which, as far as the pain is concerned, is not to be compared to acute pain observed in ulcers and cancer. Sometimes, as in the form described by See and Mathieu, painful crises precede the moment when the dilatation becomes appreciable; the same may be said of the dilatation following on Reichmann's disease. Lastly, an ulcer or a cancer can add their peculiar pains to the somewhat painful sensation which exists when the stomach is not emptied, for any reason. Gaseous Dicharges-.— When the dilatation is not very marked, especially in neuras- thenic patients, the epigastric heaviness and the swelling give way little by little, and if the patient takes his meals at regular inter- vals, his stomach at last empties itself, and his pains disappear. But generally they cease only when vomitings more or less copious, have relieved the gastric cavity of the foods which have burdened it, sometimes for more than twenty-four hours. To this feeling of fullness are added disgusting gaseous dis- charges, often very fetid. The alimentary contents in fact are liable to set free in considerable quantity many different gases. We have cited some examples of these cases in the chapter on general symp- tomatology above, and Franz Kuhn has published a long work on this subject. The principal gases are carbonic acid, hydrogen, oxy- gen, nitrogen, carburet of hydrogen and carbonic dioxide. When- ever there is stasis, their presence may be verified by directly ex- tracting the gas from the stomach by appropriate means, or by set- ting free the gastric contents in a closed vessel, after having ex- tracted them artificially. The causes of this gaseous development are supposed to be the presence of fungi resisting the antiseptic action of the hydrochloric acid even when present in excess, the fungi have been isolated and cultivated; they may be associated with a great number of other kinds of fungi when the contents of the stomach become neutral or alkaline. These fermentations, which are very frequent, are moderated by Salicylic acid or sacchar- ine; boric acid, carbolic acid; — creosote and chlorine water have no effect except in doses which are incompatible with their therapeutic — $7 — use. The great quantity of liquid contained in the stomach facili- tates the development of anaerobic germs, giving rise to products of fermentation, more complex and perhaps more poisonous. Pyrosis: — The regurgitation of a certain quantity of liquid often accom- panies the gas discharges which pass through the cardia, and pyro- sis which, as we have seen, results from contact of the majority of the neutral, acid or alkaline gastric liquids, with the wall of the oesophagus, is often added to the other phenomena which torment the patient. Vomiting:— However, the gas discharges and the pyrosis are relieved, just as the sensation of fulness is, by the emesis which relieves the stomach of its contents. They are not as frequent as they are at certain stages of the development of cancer or of ulcer; they are generally separated from each other by a variable but comparatively long time, and it is rarely that they occur at the time of the maxi- mum of digestion. The following is the course which matters usu- ally take:—for one or two days a patient has suffered, after each meal, from a sensation of growing uneasiness, and from a feeling of weight at the epigastrium, more and more painful; then suddenly, often towards the middle of the night, he is seized by very abun- dant vomitings, after which he can enjoy a little rest. These vomitings are sometimes composed of several litres of a mixture of solid food, drinks and mucus. The quantity of vomited matter is a first rate symptom of dilatation, and allows it to be dis- tinguished, for instance, from simple displacements of the stomach. We have already said that chronic gastritis, cancer, etc , might give way to slight hemorrhages, and in this case,, the blood very much modified, remains a long while in the stomach: the same phenomenon will be recognized in dilatation. The permanent presence of bile and of pancreatic fluid, of which we have given the characteristics, would allow us to decide on steno- sis of the duodenum, and would be an excellent symptom of dilata- tions following on the compression of this part of the intestine by a movable kidney, for instance. Lastly, the vomited matter will have a more offensive smell, the longer it has staid in the stomach. — 88 — Later on, when the walls are distended, the vomitings come on at greater intervals; the odor of substances vomited becomes more revolting: and now the emesis is rarely sufficient to empty the stomach, the feeling of relief, which at first followed, ceases to be produced. General State of Health:— The general state of health suffers naturally from digestive disturbances, but it is more often, and more deeply influenced by the cause of the dilatation than by the dilatation itself. Diabetes, chlorosis and great pyrexias provoke general disorders, and it is difficult to distinguish from among these disturbances, that which belongs properly to gastric atony. Neurasthenia often causes an atony of the muscular fibres of the stomach, the consequences of which cannot but have a marked influence on the nutrition of the patient and encourage and develop in their turn an original neuras- thenia. There is thus produced a veritable pernicious circle in which, however, the general cause seems to play the most promi- nent part, since, as we have said with regard to dyspepsia, it is only by addressing one-self to it, that one has any chance of curing the patient. Bouchard and his pupils have seen in this simple or original dilatation the pathogenic cause of a great number of very different diseases. We have observed nothing which allows us to accept their view. We therefore cannot appreciate the value of the theo- ries which they have built up, and which are to be found remark- ably set forth in the works on general pathology by Bouchard, and the thesis of Le Gendre. Personally we hold to the idea that pathological phenomena of this kind, of which the stomach may be the seat, are most often, if not always secondary. In dilatation through an organic cause, the disturbance of the general state will vary with this cause. It is thus observed that in cancerous patients the dilatation is accompanied by the most evi- dent cachexia. In the ulcer, Reichmann's disease and chronic gas- tritis, it will only be coincident with an emaciation more or less marked. In the case of children, Moncorro and Cornby have attributed to dilatation caused by overfeeding a certain part of the develop- - 89 - ment of rachitis. The latter author also considers it to be the cause of certain convulsions, of insomnia, of ring-worms, of urticaria and of bronchitis. We have never observed anything of this kind. The state of the tongue is not necessarily in agreement with that of the gastric cavity, and if it is usually coated and white, this symptom, like many others, depends much more upon local states and on the general state of health than on the gastrectasia itself. We have spoken fully of the vaious state of the tongue in the chap- ter on chronic gastritis. Cardio—Pulmonary Symptoms:— The distention of the gastric cavity by gases in food sometimes hinders considerably the functions of the diaphragm, and disturbs the action of the respiratory apparatus and of the circulation, more or less in different cases; one meets most often with dyspnoeic phenomena, or modifications in the sound of the heart and in the rhythm of the pulse. Mattheides has gathered together a certain number of cases in which was to be observed a sensation analogous to that of globus hystericus in patients afflicted by dilatation. He has shown that this sensation was aggravated when the stomach had sunken, and diminished, on the other hand, when it had risen; he had concluded from this that the displacement of the stomach so often accom- panying the dilatation of this organ was the cause of this sensation of globus through the dragging which occurs on the oesophagus. Schmidt is said to have verified, by a laparotomy, the existence of these anatomical disorders in a patient who had previously com- plained of the sensation of globus, but our personal observations lead us to believe that there is no relation at all between dilatation of the stomach and globus hystericus. Percussion and Palpation of the Stomach:— Percussion and palpation allow us to accertain the limits of the lower edge of the great curvature, and thus to appreciate the degree of the ectasia. The percussion should be performed with the patient standing up and again lying on his back. The measured ingestion of a certain quantity of water will allow one to estimate the atony of the wall, and at the same time will furnish exact data on the dis- 90 — placement of the lower edge of the organ, which has become heavy. However, since difficulties depending on the more or less noticeable repletion of the intestine might hinder the interpretation of results, it is best to distend the stomach still further with an effervescing mixture, at the same time filling the colon by an injection. Other authors have proposed to perform the operation inversely, and per- cuss the stomach made heavy by a certain quantity of water, while the colon is distended by gas. (Ewald). It is true that these ex- cessive precautions would make mistakes very difficult. Professor Osier holds, that when the distended stomach is outlined on the wall, one can usually follow its delineations with the eye, and of course much better by percussion. In the Phila. Med. Times tor May, 1891—Pepper reports a case of dilatation caused by Schirrous of the pylorus in which there was a visible peristalsis. This gaseous distension has also the advantage that it allows the distinction to be made between true dilatation and a simple dis- placement of the organ. By palpation the splashing sound can be investigated. This is easy to perceive when the stomach, the pylorus of which is constric- ted, is full of those liquid masses already mentioned in connection with the vomitings. But when the dilatation is not very marked, the splashing becomes less clear, and Debove has recently shown that the intestinal canals when half distended by gases are capable, tinder the influence of movements comunicated by the fingers, of producing a sound so like that of the splashing, as to make the dis- tinction very difficult. Chomele had already drawn attention to this cause of mistakes, and to that which depends on the presence of liquid and gas in the large intestine: "The splashing in the stom- ach" says he, "might be confused witn a similar sound of which the large intestine is sometimes the seat, which can be produced by the lateral movement of the body, but still more easily by the pressure of the hand on the regions occupied by the colon". It is met with especially in subjects who have recently received an injection, and those who have been seized with serous diarrhoea. The knowledge of these conditions, and the particular source of the splashing sound are sufficient to distinguish it from intestinal splashing. In fact many outhors have met with a splashing sound even when, on in- troducing the probe into the stomach, they have been unable to — 91 — withdraw any liquid whatever. Jaworski has recently brought to notice four cases of this kind, and we have observed many exam- ples of it. It is not, therefore, a reliable sign, and one must guard against attaching more importance to it than it really deserves. One can also perceive the lower limit of the stomach, either by means of the sound, the end of which one seeks to feel through the abdominal wall, after having slowly advanced it as far as pos- sible; or by means of special instruments such as that invented by Ghibaut of Nancy, which consists of a probe through which slides a thread with a leaden weight. The probe is long enough to reach the cardia, and the quantity of thread taken by the leaden weight before it arrives at the bottom of the stomach, allows one to meas- ure the vertical dimension of the gastric cavity. We have described the methods of procedure based on the employment of salol, oil, iodide of potassium, etc., destined to determine the state of the motor functions and of the absorption of the mucous membrane. In dilatation, they give information of varying value, but inferior to that furnished by exploration with the sound. We have already said by what criterion we recognize atony of a muscular wall, either presence of debris of food in the morning before breakfast, or the prolonged stay, in the gastric cav- ity, of a trial meal. The Hemmeter Gastrograph is a graphic meth- od of obtaining motor records from the human stomach, and its re- sults are generally reliable. (Part 1. p. 54). Test Meals:— In order to make a patient absorb a test meal, the study of which may procure some information, care must be taken to wash the gastric cavity, on the evening of the day before. The substan- ces extracted by this preliminary injection are sometimes very abun- dant and having the same composition as those vomited, generally become separated, when allowed to stand, into three layers: an up- per one frothy and turbid, a middle one liquid, and a lower one composed of alimentary detritus of all kinds, or simply of amyla- ceous substances, as occurs in the case of patients suffering from hyperacidity. With the microscope, ferments and sarcinae will be discovered, and all the series of products which can, normally or abnormally, be contained in the stomach. - 92 — In the morning before breakfast, the gastric cavity, which has been previously cleansed the evening before, may again contain products of secretion, which are acid, (gastrosuccorrhea) neutral or rich in mucus, (chronic gastritis, and alcoholism). The digestion of the test meal will be generally slow, and especially in cases of cancer, it will be impossible to detect free hydrochloric acid. In other patients a normal or exaggerated state of secretion of a hy- drochloric acid will be found. In all cases the appropriate re-agents allow us to recognize the presence in excess, of lactic acid, and fatty acid products. Constipation:— To these already numerous symptoms are to be added those which come from the state of the intestines. Constipation is fre- quent and obstinate, and not only are the stools rare, but the quan- tity of substances evacuated is also much less than in the normal state. This is a very valuable indication, for it shows the approxi- mate amount of food which passes into the intestine. Thus Kuss- maul had already been able to establish the prognosis of the pa^ tients attended by him, according as, in treating the dilatations, the normal course of the food substances was re-established or not. The latter state indicates an incurable stenosis of the pylorus. State of the Urine:— The urine is equally modified in quantity and in quality. The patients are in a veritable state of chronic inanition, and the urea is therefore necessarily diminished. The stomach absorbs little liquid, as the constant thirst by which these patients are tormented testi- fies; and the dilatation brings about a deficient urinary secretion. Lastly, when the dilatation accompanies an excessive secretion of hydrochloric acid, and the latter is thrown out, either by frequent vomitings, or by injections too often repeated, the urine becomes alkaline. We have alredy sufficiently developed this special uro- logy, in the first part of this work. Diagnosis:— The diagnosis of dilatation of the stomach, results from the study of the various symptoms analyzed above, and it seems diffi- cult for a mistake to occur if several of them are observed simul- - 93 - taneously. However, no sign, unless it is the presence in notable quantity of food in the stomach before breakfast, is pathognomic; still when one meets with the other symptoms singly, one is much more liable to admit a dilatation which does not really exist, than to misunderstand one which has remained latent. In order to make the diagnosis more easy, recourse has been had too strange and sometimes dangerous methods of procedure. It is thus that Bugge had the idea of recommending the following operation; he deter- mines by percussion, the patient standing up, the lower edge of the stomach, and drives the needle of a pravaz syringe above the dis- covered limit. If the liquid extracted is acid, the stomach has really been reached. Rosenbach, in order to measure the energy of a gas- tric musculature, when the dilatation is as yet hardly outlined, seeks to fix the level of the liquid contained or poured into the organ. Starting with the idea that the ascent or descent of the surface of the liquid furnishes the best information on the contractile power of thestomach. When the quantity of water deposited overcomes this force, the level is lowered in spite of the quantity of this wa- ter; in the contrary case it rises, so that it can be seen in any cavity whether it is formed of extensible walls or not. To ascertain the limits of the level, Rosenbach auscultates the stomach in the fol- lowing way; by means of a rubber ball, he makes a few bubbles of air enter the stomach, by force, through the tube. When the lower orifice plunges into the liquid, a loud bubbling sound is produced, sometimes metallic. If the orifice remains above the liquid, noth- ing is heard but the whistling of the air expelled. It is enough then to withdraw or advance the probe, to know whether the level rises or falls when water is added and at the same time, to measure the lowering of the great curvature. In an individual whose stomach is dilated, 500 cubic centimeters of liquid, cause only an insensible elevation of the level; 1000 cubic centimeters sometimes cause it to fall; on the contrary in healthy individuals, this phenomenon only occurs if ingestion of the liquid masses is sudden. Sigmund Pur- jerz has proposed to adapt a manometer to the tube; while the ex- tremity of the latter is in the oesophagus, one verifies negative va- riations of pressure. It becomes positive when the cardia is passed; this moment is noted, and also the one when the probe cannot be pushed any further. The length of tube that was necessary to use — 94 — measures the vertical dimension of the gastric cavity. It must be agreed that these methods, although interesting as physical experiments, are not very practical, and we prefer the simple exploration by means of the sound, associated or not, with the artificial gaseous distension of the stomach. These methods, in fact, suffice, and more than suffice to distinguish a dilated stomach from a displaced stomach, and from a naturally large stomach. But if they do not the following methods of Einhorn and Hemmeter will leave no room for doubt. Gatroptosis—Displacement of the Stomach:— The pylorus may be displaced, and freely movable below the epigastric region, without in reality causing any gastric disturbance. One perceives, by palpation and percussion, the great curvature of the stomach below the umbillicus. One might then be very much disposed to affirm it to be dilated, while, by setting free carbonic acid in the gastric cavity, one sees not only the great, but also the small curvature outlined under the skin, and one can trace the out- line of the whole stomach, on the abdominal wall, following the limits of the corresponding sonorous zone. This dislocation of the pylorus, frequent in neurasthenic patients, which Ewald has em- phasized, and which we ourselves have had occasion to observe several times, is one of the reasons which causes dilatation to be so easily diagnosed in these patients, who think their stomach is suf- fering when it is not diseased. One cannot be certain of this dis- placement without making use of effervescing mixtures and the electro-diaphane or the Hemmeter intragastric bag; by these it is to be distinguished from cases of megalogastria. In both cases the stomach is empty in the morning before breakfast; but in those where there is a lowering of the pylorus, one finds, on using the different means of exploration, a lowering of the great curvature, whilst the small one has kept its normal relations. In both circum- stances evacuation of the stomach, in the lapse of a normal time, indicates that the tonicity of the muscle is preserved. The differential diagnosis between gastroptosis or prolapsus of the stomach, gastrectasia or dilatation and megalogastria or large stomach (giant stomach) can be facilitated by distending the or- gan with air or gas, but even here the success, inspection, palpation - 95 — and percussion will depend upon the thickness and resistance of the external abdominal wall. Where there is very little or no emacia- tion, it is by no means easy to palpate through the abdominal wall. Then again much gas escapes into the intestine when the stomach is distended by effervescent mixtures. But by means of the stcmach-shaped intragastric rubber bag, which was described on page 54, or by Einhorn's electro-diaphane (page 78) it is possible to make the differential diagnosis without much difficulty. By Hemmeter's apparatus, which was originally designed to obtain records of the gastric peristalsis, it is also pos- sible to measure the capacity of the stomach by determining the amount of air required to distend it within the stomach (see first part on this subject). It was first used for this purpose by Schreiber of Konigsberg. This will at once enable one to diagnose a dilated stomach from one which has prolapsed but retained its normal capacity. Einhorn's diaphane is a practical method for demonstrating these two conditions to the eye. The Roentgen rays are also available for the same purpose as 1 have demonstrated (Boston Mdieal and Surgical Journal, I896). The greater curvature may be outlined by photographing a metallic spi- ral electrode that has been introduced and made to apply along the greater curvature, according to suggestions first made by Wegele; or the stomach may be photographed into by my me thod, which consists in distending the stomach by my intragastric stomach- shaped bag, the inner surface of which has been previously coated by a deposit of plumbic acetate or nitrate of silver, which is poured into the bag in a saturated solution, and allowed to dry on the in- side. The bag is then introduced and distended by air filling out exactly the entire stomach. The thin coating of plumbic acetate cuts off the Roentgen rays sufficiently to obtain a photograph. This method is troublesome, and can be satisfactorily executed only in hospital practice. For private practice the Einhorn electro-diaphane is most expedient, as it permits of a diagnosis to be made by in- spection. Debove and Remond (Maladies de 1' estomac, p. 87) state that this method is difficult of execution, and imposes much suffering upon the patient. From what we have seen almost weekly with Einhorn's apparatus, we differ emphatically from these obser- vers, and believe a further experience with the apparatus will effect a change in their opinion. - 96 - Diagnosis of the Cause:— When one is quite certain that it is a case of dilatation, there still remains to diagnose the cause of this dilatation. The former history of the patient, the examination of the sub- stances vomited, and the results furnished by a test meal, would then provide the principal data. The representations differ, in fact, considerably according as one finds a dilatation of cancerous origin, or one caused by ulcer or gastritis. A former poison and inveterate alcoholism will make one think of a cicatricial adhesion of the pylorus, of that particular atony of the submucosa, that one finds in chronic gastritis. Lastly, in studying the test meal, if there is hydrochloric acid in normal or excessive quantity one can elimi- nate cancer with almost certainty, especially if the substances vom- ited contain, at the same time, bile. If the bile is always wanting in the substances vomited, or in the gastric contents, either before or after eating, one will have a right to think of constriction of the pylorus; the latter will probably be of a cancerous origin, if the hydrochloric acid were wanting at the same time. On the contrary, the constant presence of bile and of pancrea- tic juice in the stomach would be a proof that the dilatation is a consequence of an occlusion of the duodenum, below Vater's am- pulla; this occlusion may result from a movable kidney, a fibrous adhesion, gall stones, pancreatic neoplasm, etc. One can then discover, in this way, whether the pylorus is the seat of an obstacle, or whether it is passable, and lastly, what is the probable nature of this obstacle. The accuracy of these results, it is true, is by no means absolute, but in practice, in asssociating them with other data furnished by the elements of the diagnosis of each gastric affection, one arrives at a largely sufficient approximation. A stenosis of the duodenum can be definitely ascertained by my method of duodenal intubation (see part 1. p. 31). Prognosis:— The evolution of the disease which occupies us, varies according to the cause; when it is a case of simple atony of recent date, a proper treatment of which we shall speak again further on, may bring amelioration rapidly, and even cure. But when it is a case of dilatation with atrophy of the muscular coat, especially when there - 97 — exists an impassable obstacle at the pylorus, the cure is impossible, except sometimes by operation. The treatment still relieves the painful phenomena but the inanition makes progress from day to day, and the patient succumbs to inanition, unless one of the complica- tions that we have mentioned comes and hastens the end. Malformation of the Gastric Cavity:— Dilatation is, in reality, a deformity of the stomach. Under this head comes the study of a certain number of cases in which malformations or changes of form, of the most varied kind, have been verified. Atresia of the gastric cavity, results from diminution of work by the organ, through insufficiency of alimentary contributions. Inanition and constriction of the oesophagus or of the cardia, will thus have been the first cause of this atrophy. In other cases it is a cancerous infiltration extended over the whole wall, a chronic gas- tritis with hypertrophy of the submucosa, and of the connective tissue (Linitis plastica), or a fibrous, deforming peritonitis, which will have played the same part. The calibre of the stomach thus narrowed sometimes does not exceed that of the intestine. When the upper digestive paths are open, vomitings occur which appear as soon as the quantity of food exceeds the very small volume that the stomach can contain, and the small calibre of this organ, be- comes still more clear when one comes to distending it with car- bonic acid. If stenosis of the oesophagus, or of the cardia, exists, the passage of the probe becomes impossible, and the symptoms of these constrictions assume enough importance to obscure entirely those which might be furnished by.the state of the stomach. The Hour-Glass Stomach:— Cicatrization from an ulcer, or from the loss of any substance, may bring about malformations which will present, in some cases, an analogous appearance to certain congenital malformations. Sto- ker has published one of these cases, where the stomach, divided into two parts by a congenital furrow, had never during life, pre- sented any functional disturbance. Iago has related the story of a patient who succumbed when 42 years old, after having presented for ten months, uncontrollable vomitings; on the examination of — 98 — the abdomen, there was found, underneath the liver, a soft tumor which had been taken for the right displaced kidney. There exis- ted no tumor at the level of the pylorus; the vomitings took place without pain, and were not preceded by regurgitation, there was no cachexia to be found. At the autopsy there was found a stomach presenting two dilated sacks which communicated by a closed nar- row passage situated about the middle of the organ; the index fin- ger could not pass this constriction; the cicatrices which had pro- duced this deformity, must have been caused by a former disease which appeared at the age of 30, and was characterized by hemate- mesis and acute pains. A patient of 50 years old, observed by Luigi Mazotti, experienced such intense pains, after meals, that she used to squirm on her bed, and only found little relief after having vomited everything that she had just taken. At the autopsy, the stomach was found divided into two parts: the upper one vertical, the lower one, directed horizontally towards the right side; a nar- row passage was situated between the two parts. The lower por- tion of the stomach, had made a complete circle, and the contracted point was exactly the centre around which this rotation had occur- ed. The upper part of the stomach was distended by gases; the lower one was empty and joined to the abdominal wall by some adhesions. When the viscus had been replaced in its normal posi- tion, it was found that neither the orifices nor the wall presented any modification, and it was impossible to discover the cause of this displacement. Chiari suspected a cancerous constriction of the py- lorus, in a patient who, in reality, had an intussusception of the stomach into the duodenum. These cases are rare, and could not be diagnosed. It is suffi- cient, therefore, for us to have mentioned them. Details could be found in the recent memoirs of Bauermeister and Saundby and in the thesis of Kern. (Inaug. Dissect. Berlin, 1881). Chiari (Wien Med. Wochsehr., No. 42, 1890). Bauermeister (Inaug. Dissect. Halle, 1790). — 99 — TREATMENT OF MOTOR INSUFFICIENCY OF the FIRST DEGREE -- GASTRIC ATONY OR MYASTHENIA. PROPHYLAXIS:— The muscularis of the digestive organs may be weak by in- heritance. Chlorosis, Anaemia, Tuberculosis and Cholelithiasis, ex- hausting hemorrhages, infectious diseases, typhoid, malaria diph- theria influenza may bring on myasthenia and frequent and rapidly consecutive births may by causing increase of space in the aedomi- nal cavity and loss of tone to the abdominal muscles — lead up to gastric atony. Bad chewing, hasting eating and deglution, defective teeth must have their correction. The treatment in all cases must seek and adapt itself to removal of the cause. Anaemia must be treated by proper food, peptonate of iron, bone marrow and arsenic. In ladies with gastroptosis and atony, the abdominal muscles must be strengthened and supported by proper bandages. The treatment proper includes diet, hydropathic, electric proceed tires, massage and medicines. Diet:— Patients with gastric atony must eat frequently but very little at a time. As water is not absorbed from the stomach the quantity of liquids must not exceed 1 - lj4 quarts in 24 hours, including all drinks, coffee, soups, etc. Where there is a craving for more liquid than this, it should be introduced by enema. Milk Cures:— My experience with the frequent and peristent administration of milk as observed in milk cure sanitariums in Germany is dis- couraging. 1 believe this treatment to be a useless dietetic experi- ment in gastric atony. The special diet must be selected according to the state of the gastric secretions. If there is hyperacidity, I recommend a vigo- rous beef and mutton diet with limited carbohydrates, hard and soft boiled eggs, ham, tongue, oysters, duck, deer in every form; of vegetables, I allow carrots, spinach, soft boiled turnips, beans, peas, cauliflower. Potatoe, macaroni, rice and farina gruel are permissable. — 100 I am not too strict concerning alcoholics, and where a trial proves that they aid digestion, I generally permit claret, rhine wine, and even small amounts of good beer, not more than 300 cc. or Y>, pint a day. Whenever the hydrochloric acid is diminished, the lighter meat varieties, chicken, pigeon, birds and fish should be al- lowed only, but a larger amount of carbohydrates conceded. Constipation is a serious cause and constant accompaniment of gastric atony; it must therefore receive the most undivided atten- tion. Purgatives should be used only as a last resort and the main reliance placed on diet. A pint of cold water in the morning on an empty stomach, black or graham bread, abundance of vegeta- bles—turnips, carrots, asparagus, tomatoes, rhubarb plant, beans, peas, lenitls, noodles, macaroni, barley, sweet compots, plums, figs, apples, currents, cramberries, cider. Sweeten everything with milk, sugar, butter-milk, kefir, sourmilk, honey. An abundance of these articles very rarely fails to bring about regular passages without medicines. Whenever a drug is positively unavoidable, I prefer cascara segrada. In pronounced atony, constipation can not be treated by this diet only, because it increases the weight of ingesta. The hydropathic treatment consists in cold morning sponge baths, cold wet packs and Pnessnitz bandages to epigastrium. I am in the habit of ordering a daily bath in severe neurasthenic myas- thenia which contains 3$ chloride of sodium and 2$ sodium bicar- . bonate;—temperature of bath 98°;—to remain in 20 minutes. Electric Treatment:— Intragastric, with the Einhorn electrode (Hemmeter's modifi- cation) in the stomach; the faradic current is applied up and down over the spinal colum and over the abdominal muscles. The con- stant current is applied in the same manner in the strength of 20 milliamperes and for about 10 minutes Systematic massage both general and local over the stomach is an important adjuvant. Medicinal:— This form of treatment should be as limited as possible. The most approved tonic for the motor function is strychnin. — 101 — B Strychnin Sulphatis gr. y„ Elixir gentians cum Ferri chloride, gvi M.fl.gss t.i.d. Where the hydrochloric acid is deficient it must be supplied where it is excessive it must be neutralized by the following-— B Magnes. ust. 150 Bismuth Carbonic. Natron bicarbonat. a.a. 5.0 Extract Strychni 0.1. M. Y teaspoonful one half an hour after meals. Creosote and orexin are claimed by competent authorities (Pick and Penzoldt) to be able to excite the peristalsis; the latter may be used where there is an or subacidity. Lavage:— As a rule one will be able to get along without lavage in the first stage of motor insufficiency. But where the food remains in persistently over time, I have seen improvement of muscular toni- city follow the rapidly alternating cold and warm intragastric douche; this exerts a powerful and stimulating effect also on the secretion when it is defective, when the latter is excessive the douch- ing should be carried out with alcaline water. TREATMENT OF MOTOR INSUFFICIENCY OF THE SECOND DEGREE — FULLY DEVELOPED DILATATION. This may be considered under two headings;— (1) Medical, (2) Surgical. The Diet is essentially based on the same principles as in simple myasthenia; the amount of permissible liquid must not exceed 1500 c.c. in 24 hours. With exaggerated vomiting and pains, I would recommend exclusive feeding by the rectum for 14 days. A specified diet list for both simple atony and pronounced dilata- tation will be appended. It is impossible to treat the latter form successfully without lavage, this is not only a palliative measure of great value, but in cases of atonic dilatation due to muscular weak- — 102 — ness and not dependent upon mechanical obstruction, it may even be able to effect a cure when combined with other means, presently to be described. The first washings are carried out with pure warm water, but the last ones are done with solutions adapted to the chemical and septic state present in the organ. For instance, if there is great ex- cess of hydrochloric acid and fermentation by sarcinae and yeast, Sodium biborate or bicarbonate should be added, as these are not only antiacid but with regard to these organized ferments, antiseptic. If there is butyric or lactic acid fermentation, Boracic acid, 3$— Salicylic acid, 0.3$—Creolin or Lysol 10-15 drops to a quart should be used: But the stagnation can not be prevented from re- curring by these means unless the motility is improved by other treatment. Electricity should be employed externally and internally as described in previous chapter. Massage undoubtedly improves the gastric musculature but should only be used on days when the stomach has been washed out, because the mechanical compression may force stagnating mas- ses into the intestines, thus spreading the putrefaction. Abdomi- nal bandages properly adapted and applied have proven a valuable palliative measure. Hpdrotherapeutic applications are indispensable and should be used as described in the last paragraph. Medicinal Treatment has a twofold object; (1) To promote the motor function, (2) To prevent as far as is possible, gastric fer- mentation and decomposition. The only drug in which I have any faith for improving gastric peristalsis is strychnin sulphate, it should be given in heavy doses, not less than I-30 grain for adults, t.i.d. Boas combines strychnin with an antifermentative in the fol- fowing manner;— B Extract strychnin Codein phosphoric. a.a. O.03 Bismuth salicylici basic 0.5 Sig. M. Make into 20 powders, one powder after each meal. F. Kuhn has proposed salicylic acid 0.5 grm. per dose—Salicy- late of sodium, 15 - 30 grains—Saccharin and Sodium benzoate, of — 103 — each form 10 - 30 grains per dose to counteract gastric fermenta- tation. Carbolic acid was first used by Naunyn for the same pur- pose. When there is marked lactic or butyric acid fermentation, there is not a better agent than hydrochloric acid to counteract it:- 20 - 30 drops of the dilute form in gii water, through a glass tube. Salol, Naphthol, Beta Naphthol Bismuth and Beta Naphthol Bismuth benzoate or Benzonapthol. The French are very enthusiastic con- cerning antifermentative treatment of gastrectasia, but it is certain that this treatment alone with lavage and proper diet is fallacious. Dujardin Beaumetz employs;— B Bismuth salicyl. Magnes. Usta. Sod. bicarb, a.a. 10 grm. Sig. M. To be devided into 30 powders, one powder after meals. My own formula for gastric fermentation particularly when associated with putrid Diarrhoea is;— B Beta Naphthol. Bismuth, benzoatis 3ii Bismuth Salicylatis sii Magnesiae Ustae 3ii Saccharin 3h Menthol 3ii Sig. M. To be divided either into 12 or 24 powders to suit the indica- tions; if there is much fermentation, it should be devided into 12 powders and one given 4 times daily. Otherwise it should be di- vided into 24 powders and one given every 3 hours. For vomiting, lavage is the most efficacious treatment but if it fails a hypodermic injection of morphine and atropiae sulphat will be called for. As a rule menthol and chloroform do not dissap- point when used for the relief of vomiting. The following formula is practical;— B Mentholi, gr. xvi Chloroform, gtt. xxiv Elixir simplic, q.s. fl. gii Sig. M. fl. 3ii every hour. Insomnia must sometimes be treated as — 104 — these patients imperatively need rest for this purpose Chloral gr. xv per enema is most advisable. Surgical Treatment:— The operations that have been suggested for the relief of Motor insufficiency vary according to the object to be accomplished. Mo- tor insufficiency from simple atonic dilatation may be relieved by reducing the size of the stomach by excision of a piece of the same, an operation known as Gastrorrhaphy. If the Pylorus is stenosed by a simple cicatrix or hyperplastic sphincter Loretas Digital Divulsion of the pylorus is an operation which judging from the statistics is an unsafe and unreliable pro- Ceedure. The Pyloroplastic Operation of von Heinecke — Milkulicz, which Boas terms the ideal surgery for the relief of pyloric stenosis of a benign nature produces more permanent results. There are two more, Gastroenterostomy and Resection of the pylorus. The Indications for these operations and their technique are subjects concerning which the reader must be referred to textbooks on surgery. The larger portion of dilatations is un- doubtedly due to some obstacle to the exit of thechyme(is chochy- mia as Einhorn calls it) and it is rational to presume that purely medical means can not effect a permanent cure of these conditions. But the obstructions or obstacles to the chyme are not even all found in the stomach itself, for in the account given under the etio- logy, distended gall bladder, gall stones impacted in the diverticu- lum of Vater, floating kidney, duodenal cicatrices and neoplasm peritoneal adhesions etc., have been referred to, and all of these give their separate and distinct indications for operation. — 105 — DIET FOR MOTOR INSUFFICIENCY OF the FIRST DEGREE —ATONY—MYASTHENIA. At 8 A.M. Milk 100 grms. Toast + 30 gr. Butter = 401.2 Cal. At 10 A.M. 50 gr. Wheat bread + 30 gr. Butter + 60gr. scraped beef =415.2 Cal. At 12 M. 150 gr. boiled Beef. + 50 gr. potatoe puree or macarony = 439-3 Cal. At 3 p.m. 100 gr. milk -f 50 gr. Zwieback, =401.2 Cal. At 7 p.m. 100 gr. Cold ham + 150 gr. wheat bread + 30 gr. butter =557-5 Cal. Total 22144 Cal. About 3oz. good Portwine or Claret may be allowed during the day. DIET FOR MOTOR INSUFFICIENCY OF THE SECOND DEGREE —PYLORIC STENOSIS — MYASTHENIC DILATATION. At 8 A.M. 50 gr. tea with 50 gr, milk sweetened with Saccharin, no sugar + 50 gr. toast = 195-5 Cal. At 10 A.M. 100 gr. scraped lean beef = 437.0 Cal. 30 gr. toast = 77.7 Cal. 10 gr. Butter = 71-3 Cal. Total 586.0 Cal. At 12 M. 150 gr. Roast beef = 320.7 Cal. 50 gr. potatce puree = 63.7 Cal. Total 384-4 Cal. In place of the potatce puree the same of spinach, carrots, peas or beans may be allowed in the same quantity. At 2 p.m. 50 gr. Cream = 107-3 Cal. At 4 p.m. 100 gr. Tea or coffee with Milk, no sugar, but saccharin 50 gr. Toast =195-5 Cal. — 106 — At 7 P-M 100 gr. broiled white or yellow perch or oysters = 71-75 Cal. 50 gr. Wheat bread = 129-0 Cal. 10 gr. Butter = 71-3 Cal. 100 gr. Cream =214.0 Cal. At 9 P.M. 50 gr. Cream = 162.3 Cal. Total 1885.15 Cal. In atony and dilatation as well as in carcinoma, experience is the best guide for enlarging and varying the diet. Every new ar- ticle of diet must at first be tried with great caution; If liquids are well tolerated they may be increased and soups allowed for the noon meal. The daily lavage should at times be undertaken at hours when a test meal can be secured thereby which will inciden- tally instruct the physician concerning the digestibility of new foods and what is more important the state of the motor function. — 107 - Professor J. C. Hemmeter's Synopsis or Scheme for examining Stomach Patients at THE MARYLAND GENERAL HOSPITAL. Medical No__ Name......... Address......... Age..... Color......... Sex......... Social Condition......... Diagnosis......... Date......... HEREDITARY FACTS OF IMPORTANCE. PREVIOUS HISTORY—Severe Constitutional Diseases. First appearance of symptoms and cause? Did they appear suddenly? Intenraly? Or gradually? Continuous? Or remittent? what intervals? Occupation? Habits? Alcoholism? Tobacco? Cold? Change of climate? Mental strain? Trauma? Malaria? Did it begin with or without a chill? Fever? Yellow fever? Constipation? Diarrhoea? Dysentery? Typhoid fever? PRESENT HISTORY—Diesases of other organs. Dyseptic symptoms? Pressure? Local and subjective complaints? Fullness? Pain? Distention? Restlessness? Sounds in the digestive tract? Bowel movements? Nausea? Eructation? Vomiting? Haematemesis? Appetite? Taste? Thirst? LOCAL SUBJECTIVE SYMPTOMS. Any difficulty or pain on deglutition? If so, its reg- ularity? Irregularity? Intensity? Duration? Effect of food on pain? Do they occur in every position of body? or only in certain positions? Time of onset after meals? Pain at night? On an empty stomach? Improved by eating? Exaggerated by eating? Is pain diffuse? or circumscribed? ERUCTATION—Duration? Occurring on full? or empty stomach? Is gas tasteless? Odorless? Acid? Decomposed? After what foods? Presence of pyrosis or heartburn? NAUSEA AND VOMITING—Occurs on full or empty stomach? Frequency? Taste of vomit? Appearance of matter? Food particles? Proteids? Starches? Mucous? Bile? Blood? rood eaten several days before? Does emesis relieve symptoms? APPETITE AND THIRST. Accustomed diet? Mode of life? Anorexia? Bulmia? Aversion to meat? Thirst? BOWELS—Constipation? Diarrhoea? Undigested particles of food? Mucous? Pus? Blood and source? Results of blood examination. GENERAL NUTRITION. Emaciation? Loss of weight in pounds? In what time? PHYSICAL EXAMINATION. INSPECTION. Change in form of abdomen? Tumor? Gastric or intestinal peristalsis? PALPATION—Time of examination? Temperature? Outline of stomach? Upper border? Lower border? Presence of tumor? Movement of tumor? Was stomach full or empty? Pain on pressure? Diffuse or circumscribed? Succussion sound? PERCUSSION—Limits of the stomach? DISTENTION WITH AIR OR GAS—Limits of stomach? Results with intragastric bag? Does tumor move with distension? Made more or less distinct? ELECTRO DIAPHANY—Limits of stomach. Tumor? EXAMINATION OF TEST MEALS. Double test meal of the Md. Gen. Hos. at......... Ewald breakfast at......... Contents drawn at......... Date......... MICROSCOPICAL EXAMINATION. Quantity? Color? Odor? Food particles.' Froth or gas? Mucous? Bile? Blood? CHEMICAL EXAMINATION. Reaction? Free Acid? Free HCL? Lactic acid? Amount free HCL? Combined HCL? Amount acid salts and organic acids? Total acidity? Erythro dextrin? Deficit of HCL? PEPSIN. Albumin digested in pure filtrate in...min. Albumin digested in acidified filtrate in...min. Albumin digested in HCL and pepsin filtrate in...minutes. RENNET. Milk coagulated by rennet in......min. Milk coagulated by rennet zymogen in......min. Rennet zymogen active in dilution 1: Contents after meal previous evening at 8 a.m. Contents after lavage previous evening at 8 a.m. Time of palol reaction......minutes. Time of iodide of potassium resorption test......minutes. MICROSCOPICAL EXAMINATION. Bits of tissue? Bacilli? Yeast cells? Bits of mucosa? URINE. Amount? Urea? Reaction? Indican? Performed sulphates? Albumen? Tube casts? Ethereal sulphates? Ratio? Sugar? Specific gravity? TREATMENT. Diet? Medicines? Electricity? Massage? Hydrotherapy? Lavage? Results. — 108 — INDEX. PART FIRST. ANATOMY, PHYSIOLOGY — TECHNICS OF DIAGNOSIS. /\natomy, intestines small 9 large 19 Absorption from stomach 68-73 Antrum pylori 61 Analysis of gastric contents 116 Action of pepsin on proteids 144 LJile, analysis and function 38 Bacteria 40,47 Biuret reaction 28 C 1 cecum 19 Colon 3 Composition of gastric chyme 43 Carbohydrate fermentation 45 Cell structure of peptic glands 7 Chemical analysis of gastric juice 122 L/istension of intra-gastric bag 32 Duodenal intubation 31 " illumination Digestive properties of gastric juice 29 Digestive properties of duodenal juices 44 Digestion of albumens 28 " " starches 24,35 " physiology 20, 30 Duodenum 17 Digestive ferments 139 Emu lsitication of fats 35 Effect of electricity on the stomach 58 Examination of stomach con- tents for bacteria, mucosa, blood, bile, etc. 93 Ferments, fate of digestive ferments 47 gastric 26 intestinal 34 organized 39 unorganized 35 Ljlands of intestines 15 " " stomach 6 Gastric secretion 26 motility 57,62,67 " disturbances by bacteria 96 Gastro-diaphany of Einhorn 77 H istology, stomach intestines Hemmeter's method 1 ntestinal putrefaction Indol Jej unum 7 13,20 54 39,46 36,40 ■ 19 90, 103 82 Literature Lavage, indications and contra-indications 84 / Vlotor function of stomach 49 N erve supply of stomach 6 " intestines 17 — 109 - V_yrigin of Hcl. 26 Oppler-Boas bacillus 95 1 ylorus 2 Pancreas 3 its secretion 34 Pepsin 28 test for presence of \Juantitative analysis stomach 141 of aci< is: Rennet and rennet zymogen 30 test for 143 Otomach 1 method of distension 74 " " location 74 demonstration of tumors in and out of 75 transillumination 78 secretion into empty 113 Steapsin 35 Separation of albumins 144 Topfer's method 131 Martius and Luttke 133, 135 Leo's method 135 Boas' " 137 total fatty & organic acids 138 R A elative pressure of peristalsis 66 T, rypsin 36 Tests 29, 50 and 123 to 146 Test meals 87 withdrawal of 76 V ill! Vermiform appendix 12, 16 19 PART SECOND. THE GASTRIC CLINIC. cute gastritis 1 diagnosis 16 duration 15 etiology 7 pathological histology 10 prognosis 16 symptomatology 13 treatment 17 Age of 607 cases of open ulcer 59 Ages of 2038 cases of gastric carcinoma 76 \_>hronic gastritis 33 diagnosis 46 etiology 35 pathological anatomy 37 " histology 41 prognosis 48 symptomatology 41 treatment 49 diet 51 Causes, mechanical and chemical 57 " interfering with the vitality of tissue 57 " bacterial infection 57 " bacterial necrobiosis 58 " thermic 58 " cutaneous burns 58 " constitutional 58 Carcinoma of the stomach 68 " " cardia 68 diagnosis 69 treatment 70 Carcinoma of fundus— anterior or posterior walls, curvatures and pylorus 71 examination of stomach contents 72 cancer arising from ulcer 73 treatment 73 diet for carcinoma 74 surgical treatment 75 morbid anatomy 77 — 110 — D; 'ilatation—gastrectasia 80 Dilatation through mechan- ical obstacles 80 without " 82 Diagnosis 59 differential diagnostic points between ulcer, gastralgia, hyperchylia and carcinoma 60 differentiation of (ulcer) gastric haematemesis from pulmonary hemorrhage 61 differentiation from cholelithiasis 62 differentiation of compli- cations and consequences of gastric ulcer 62 perforation peritonitis 63 ulcus carcinomatosum 63 hour-glass stomach 63 subphrenic abcess 63 Etiology Etiology 57 79 G astroptosis, displacement of stomach 94 diagnosis of the cause 96 prognosis 96 malformation of the gastric cavity 97 dilatation and hour- glass stomach 98 nfectious gastritis 26 M Lycotic gastritis 28 Motor insufficiency,! st degree 78 2nd " 79 hlegmonous gastritis 23 diagnosis 25 etiology 24 pathological histology 24 prognosis 26 symptomatology 25 treatment 26 Pathological anatomy 84 Oymptoms 85 state of appetite 85 pain 86 gaseous discharges 86 pyrosis 87 vomiting 87 general state of health 88 cardio pulmonary 89 percussion and palpation of the stomach 89 test meals 91 constipation 92 state of the urine 92 diagnosis 94 Synopsis and schedule for clinical history of stomach patients 107 I oxic gastritis 30 diagnosis 31 pathology 30 prognosis 31 symptomatology 31 treatment 31 Treatment 64 of haematemesis .64 Leube-Ziemssen rest cure 65 dietetic, medicinal and 66 surgical 67 Treatment of motor insuf- ficiency of first degree- gastric atony, etc., 99 diet 99 milk cures 99 hydropathic, electric and 100 medicinal 101 Treatment, second degree- fully developed dilatation 101 diet 101 electricity, massage, med. 102 surgical 105 diet list for both classes 105 U leer of stomach 55 self digestion of stomach 56 ^&±?& W*:« v NLM001362386