LIBRARY OF THE University of Illinois. CLASS. BOOK. VOLUME). Accession No. ✓ - tf ^ ' LIBRARY OF THE UNIVERSITY af ILLINOIS. Small capillary vein in the inter- glandular con- nective tissue, between first and second gland tubule. Capillary. Small vein 'aris- ing from muscu- laris mucosae in center of the drawing. Longitudinal and cross-section of the museularis Mucoid degener- ation of free ends of cylindri- cal epithelium. Cylindrical epi- thelium of the gastric surface. Vestibule (Vorraum.) Exit of gland duct. The darker stained are the parietal, border or oxyntic cells,* showing commu- nication with the central gland duct. The lighter are the central, chief or ferment cells. Break in contin- uity of central duct, due to curv- ing away of the gland tubule =, from the plane of .section. Between the longitudinal tu- bules 2 cross and 2 tangent sec- tions of peptic Fibres of the museularis mu- cosae embracing base of the peptic gland. HEMMETER DEI/. Hoen & Co., Lith. VERTICAL SECTION THROUGH NORMAL HUMAN GASTRIC MUCOSA. DISEASES OF THE STOMACH THEIR SPECIAL PATHOLOGY, DIAGNOSIS, AND TREATMENT, WITH SECTIONS ON ANATOMY, PHYSIOLOGY, CHEMI- CAL AND MICROSCOPICAL EXAMINATION OF STOMACH CONTENTS, DIETETICS, SUR- GERY OF THE STOMACH, ETC. BY JOHN C. HEMMETER, M.D., Philos.D. PROFESSOR IN THE MEDICAL DEPARTMENT OF THE UNIVERSITY OF MARYLAND, BALTIMORE; CONSULTANT TO THE UNIVERSITY HOSPITAL, AND DIRECTOR OF THE CLINICAL LABORATORY, ETC. WITH MANY ORIGINAL ILLUSTRATIONS A NUMBER OF WHICH ARE IN COLORS AND A LITHOGRAPH FRONTISPIECE Seconfc jEnlaroefr anfc IRevtsefc BMtion WITH NEW CHAPTERS AND ADDITIONAL ILLUSTRATIONS PHILADELPHIA P. BLAKISTON’S SON & CO. IOI2 WALNUT STREET 1900 Copyright, 1900, by P. Blakiston’s Son & Co. PRESS OF WM. F. FELL & CO., 1220-24 Sansom Street, PHILADELPHIA. o o '$ k> llo, 33 H 3 7 d 2- REMOTE STORAGE THE BELLY AND THE MEMBERS The members of the body rebelled against the Belly, and said, “Why should we be perpetually engaged in administer- ing to your wants, while you do nothing but take your rest and enjoy yourself in luxury and self-indulgence?” The members carried out their resolve, and- refused their assistance to the Belly. The whole body quickly became debilitated, and the hands, feet, mouth, and eyes, when too late, repented of their folly. — AUsop. tJ cn X -x mo?. TO PROFESSOR WILLIAM OSLER, M.D., OF BALTIMORE (II maestro di color che sanno. — Dante), THIS VOLUME IS RESPECTFULLY DEDICATED. * PREFACE TO SECOND EDITION. The exhaustion of the first edition of this book made a call for a revision necessary in a little over one year from the date of its pub- lication. Owing, however, to serious illness in the author’s im- mediate family, it was impossible to comply promptly with the request of the publishers. The whole book has been gone over critically four times by the author and his associate, Dr. Harry Adler, and there are probably not fifty pages in which some im- portant insertion or alteration has not been made. About two- thirds of the book has been actually reconstructed, and a large amount of new material added, of which the following articles are the most important: Hypertrophic Stenosis of the Pylorus, Obstruction of the Orifices, The Use and Abuse of Rest and Exer- cise in the Treatment of Digestive Diseases, part of the chapter on Motor Insufficiency, Electrodiaphany, Hemorrhage from Stomach, and the articles on Gastroptosis and Enteroptosis have been en- tirely rewritten. New illustrations and plates, being the work of Mr. Louis Schmidt and Mr. Herman Becker, have been inserted on the fol- lowing subjects: Hypertrophic Stenosis of the Pylorus from Chronic Stenosing Gastritis ; Actual Size and Configuration of the Stomach in a State of Hyperplastic Stenosing Gastritis ; Malforma- tion and Distortion of Thorax and Stomach Caused by Lacing, Tight Clothing, etc. ; Adhesions Causing Motor Insufficiency ; Gastric Distention by C0 2 , Showing the Stomach in a State of Gastroptosis ; Connective-tissue Hyperplasia Separating Remnants of Peptic Glands; Detachment of Secretory Cells; Mechanism Effecting Vertical Position of the Stomach. A text-book that undergoes subsequent editions is the product of the evolution of thought, not only of its author, but of that part of the medical profession which is active in its special domain. While the book bears the impress of the author’s individuality, it vii Vlll PREFACE TO SECOND EDITION. should, if possible, be an exponent of the total practical knowledge that has been gained. As Riegel says, “ The final object of all medical activity is to help and to heal. The practitioner has the right to estimate the progress in any domain of medicine by the gain that has accrued to the healing art.” In the author’s opinion the most useful feature of this second edition is the repeated and thorough application of mature and critical judgment to the entire subject-matter of the book. It is not intended that this should be a scientific work in the technical sense of the term, the question that weighed most heavily upon the author’s conscience being, “ How much can I aid the practitioner in his efforts toward helping and healing others?” I am indebted to the distinguished American clinician, to whom this book is dedicated, Professor William Osier, for much cordial encouragement and many useful suggestions, given both person- ally and by correspondence. To my associate, Dr. Harry Adler, I wish to express thanks for the unceasing vigilance which he exercised in the proof-reading and for the application of conserva- tive critical judgment throughout the entire book, and especially to the paragraphs on Clinical Pathology. To Dr. F. P. Mall for advice relating to chapter on the Anatomy of the Digestive Organs. To Dr. Edward L. Whitney I am indebted for rewriting the chemical section of Part I. To Dr. Henry W. Nolte (now of Newark, N. J.) and Mr. Thomas H. Cannon for arranging the index of subjects and index of authors. To the medical faculty of the University of Maryland I am indebted for the unrestricted use of the clinical and pathological material of the University Hospital and their generous support of the clinical laboratory, in which much of the newer material was clinically and experimentally tested. The almost daily association with clinicians of experience and ability gives a feeling of enthusiasm, which is a powerful auxiliary to an author, and marvelously diminishes his toil ; in the language of Ovid — “ Scribentem juvat ipse favor, minuitque laborem ; Cumque suo crescens pectora fervet opus.” The Author. Baltimore, March., igoo. PREFACE TO FIRST EDITION. The tendency of modern science — not only of medical science — is toward specialization. Diseases of the stomach alone is not a field sufficiently large to constitute a genuine specialty. It is generally associated with the study of the diseases of all digestive organs, particularly of the intestines, liver, and pancreas. The diseases of metabolism consti- tute a legitimate field naturally falling into the domain of the digestive clinical pathologist. In an address before the Medical and Chirurgical State Faculty of Maryland in April, 1896, Professor Da Costa, in 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 par- ticular 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 attempt has been made to do justice to the work of American clinicians in this special department. My chief effort has been to furnish the general practitioner with a work from which he can readily acquaint himself with all that has been done in this important branch of medicine, to fit himself to make exam- inations, to take advantage of new methods of diagnosis, and to treat this very difficult class of diseases rationally and successfully. With this end in view I have endeavored to treat the subject systematically and concisely, giving first the special anatomy and physiology of the digestive organs, methods of diagnosis and general therapy, including dietetics, following this by a methodical discussion of the various diseases affecting the stomach, with their symptomatology, diagnosis, prognosis, pathology, and treatment. ix X PREFACE TO FIRST EDITION. The illustrations, of which many are from original drawings, have been selected because of their practical bearing upon the matter in hand. Aside from the fact that the pathology, diagnosis, and therapy of diseases of the human organs have become so extensive that it is absolutely impossible for one mind to master them all, genuine advances in any particular department have hitherto been made only by such scholars as could concentrate and focus their mental energy upon a limited subject. Experience of the last twenty-five years has demonstrated that the general, fundamental stock of medical knowledge has not been injured, but, on the contrary, it has been wonderfully enlarged and strengthened by the progress in strictly special fields of work. To read the history of the development of medical sciences, the frequently astonishing results and indefatigable perseverance of “ the grand old men of medicine,” is not only a healthy training for prospective investigators, but can not fail to polish down the pride of the overambitious. Speaking purely from a therapeutic standpoint, however, our medical ancestors of the beginning of this century were for the greater part divided into two extreme classes : First, the poly- pharmacists ; second, the skeptics, the therapeutic nihilists. It is largely the credit of the specialties that Asclepiads have evolved from this confused opposition. It was an unspeakable comfort to be reassured by Virchow and others that, after all, the end object, the fundamental purpose, of all medical progress must be the relief of suffering and the cure of disease, not simply the development of abstract science. A further step in the evolution of therapy was the realization that the object of medical study and treatment must not be the “ disease,” but the diseased patient. Specialties can not make the adept one-sided, nor obscure his view of the general body of medical knowledge; on the contrary, the detailed development of the intellect which results from concentration of energy upon one subject will enlarge his powers of observation and analysis and insure a more comprehensive understanding of the totality of general medicine. Boerhaave could claim to be master of all applied medical branches; Langenbeck and Frerichs were credited with absolute mastership in three or four hetero- geneous branches of medicine. Medicine has been enormously developed since those days. Who will claim such mastery at the present time? Bach, Mozart, and Haydn were acknowledged PREFACE TO FIRST EDITION. XI virtuosi on five or six instruments. Where is such a phenomenal genius of the present day in music ? The enlargement of any branch of human knowledge or art brings specialization with it as a natural sequence; that this tendency is a blessing for the central, fundamental stock of knowledge, science, or art has been proved in many branches. Perhaps as good an evidence of this fact as any is the advantage which general medicine is just begin- ning to reap from the brilliant results of bacteriology. When the printing of this book was begun, there was no work of American origin on this subject. Since then the volume by Einhorn has appeared, being a compilation of the monographs by this author in the “Twentieth Century Practice of Medicine.” 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 Fitz are as well known in this department in our country as those of Kussmaul, Senator, Nothnagel, Leube, Ewald, and Boas in Germany, or Hayem, Bouveret, Debove, and Mathieu in France. Among those who have made contributions of note to this special line of work are S. Meltzer, Einhorn, George Dock, W. D. Booker, Charles G. Stockton, Allen Jones, D. D. Stewart, Julius Frieden- wald, Francis P. Kinnicut, F. B. Turck, Charles E. Simon, and other gifted experimenters and clinicians. The anatomy of the stomach has received a lasting benefit through the intellect of F. Mall, of Baltimore. The surgery of the alimentary tract has many very creditable representatives in our country, among whom may be mentioned W. W. Keen, Robert F. Weir, N. Senn, John B. Deaver, McBurney, Roswell Park, F. Lang, R. Abbe, W. Meyer, Murphy, Bull, Maurice H. Richardson, W. S. Halsted, Gerster, and John M. T. Finney. The literary and practical contributions of a number of these men have reached a classic standard and compelled foreign admiration. The physiological chemistry of digestion and internal secretion has received the benefit of the work of Bowditch, Chittenden, Howell, Vaughn, Adami, Able, and others, and dietetics has its versatile representative in Gilman Thompson. To Messrs. Blakiston, Son & Co., the publishers, the author feels sincerely grateful. It would be a neglect to omit an expression of this feeling. The manner in which they have executed their part Xll PREFACE TO FIRST EDITION. of the work speaks for itself. It is a great pleasure for an author to be able to work with such intelligent and enthusiastic pub- lishers. To Dr. Edward L. Whitney, my associate, it becomes my pleasant duty to express thanks for the able manner in which he has written the chemical section of part first, and also for much kind assistance throughout 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, but the land to be explored is exceedingly large in its extent, and “ the harvest is plenteous , but the laborers are few!' JOHN C. HEMMETER. Baltimore, 1897. “ Heard are the voices, Heard are the sages, The worlds and the ages ; Choose 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. LIST OF ILLUSTRATIONS PLATE PAGE Normal Histology of the Gastric Mucosa, Frontispiece. I. Three Sections of Stomach-walls Placed Side by Side to Show the Positions of Blood-vessels and Lymphatics to the Different Layers (Colored), . Opposite Page 28 II. Reconstruction of a Small Portion of the Middle Zone of the Stomach (Colored), Opposite Page 29 III. Patient with Intragastric Bag within Stomach and Pneumograph in Place, Both Connected with the Kymograph, Opposite Page 72 IV. Apparatus, not Including Kymograph, Opposite Page 73 V. Phlegmonous Gastritis in the Sequence of Ulcus Carcinomatosum, Opposite Page 434 VI. Bacterial Invasion of Gastric Epithelium. From a Case of Diphtheric Gastritis (Colored), Opposite Page 438 VII. Carcinomatous Ulcer of the Pyloric Antrum, ...... Opposite Page 490 VIII. Ulcus Carcinomatosum of the Pylorus, Opposite Page 506 IX. Syphilitic Gastritis, Showing Degeneration and Loss of the Superficial Columnar Epithelium and That of the Vestibules, etc. , . Opposite Page 596 X. Hypertrophic Stenosis of the Pylorus from Chronic (Stenosing) Gastritis, Opposite Page 618 XI. Stenosing Hypertrophic Gastritis, Actual Size and Configuration of Stom- ach Opened along the Lesser Curvature from Esophagus to Duodenum, Opposite P.age 620 XII. Malformation and Distortion of the Stomach Caused by Lacing or Tight Clothing, Belts, etc. Opposite Page 628 XIII. Gastrectasia, Transillumination of the Stomach, Opposite Page 640 XIV. Adhesions, Causing Motor Insufficiency but Retaining Stomach in Normal Position, Opposite Page 642 FIG. PAGE 1-3. Sections of Deep Ends of Fundus Glands of the Cat in Different Secretive Phases, 26 4. Plaster Casts of Duodenum of Infant and Adult, 39 5. Hemmeter’s Apparatus for Obtaining Intestinal Contents, 53 6. Pressure Bottles for Distending the Intragastric Bag during Duodenal Intuba- tion, 54 7. Intragastric Tissue Rubber Bag, with Three Distinct Parts, 80 • 8. Location of the Stomach — Dorsal View (Colored), 99 9. Location of the Stomach — Anterior View (Colored), 100 10. Normal Percussion Limits of the Adult Stomach, 101 11. Stomach Distended by Air or C0 2 , Showing Stomach in State of Gastrop- tosis, 103 XIV LIST OF ILLUSTRATIONS. FIG. 12. The Electrodiaphane, 13. Hemmeter’s Double-current Stomach Lavage Tube, 14. Illustrating the Principle of Siphonage, 15. Bulb Used for the Aspiration of Test-meals with Patients Having Very Relaxed Abdominal Walls, 16. The Esophageal Tubal Probe, 17. Stomach-pump Used Only for Rapid Evacuation of Poisons, 18. Modified Ewald Tube, with Numerous Smaller and Larger Lower Openings, . 19. Oppler-Boas Bacillus from Contents of a Carcinomatous Stomach, 20. Fragment of Mucosa Showing a Normal Condition of Glands, 21. Hypertrophy and Proliferation of Glandular Elements, 22. Atrophy and Vacuolization of Glandular Elements, etc., 23. Strauss’ Mixing Funnel for Lactic Acid Determinations, . . . 24. Gastroscope, 25. Esophagoscope, Obturator, Esophageal Forceps, Esophageal Applicator, . . . 26. Recurrent Gastric Needle Spray or Douche, 27. The Intragastric Spray, 28. Rectal Electrode, 29. Einhorn’s Intragastric Electrode, 30. Abdominal Electrode, 31. Massage of the Stomach in Dilatation or Gastroptosis, 32. Massage for Improving Gastric Tonicity, 33. Massage of the Stomach and Colon, 34. Atrophy and Vacuolization of Glandular Elements, etc., 34 A. Connective-tissue Hyperplasia Separating Remnants of Glands Which Show a Small Nucleus Surrounded by a Thin Shell of Protoplasm, 34 B. Detachment of Remnants of Secretory Cells Containing Vacuoles from Lumen of Peptic Duct, 35. Cancerous Invasion of the Glandular Layer. A Portion of the Mucous Coat, 36. Cancerous Infiltration of the Muscularis. Section of a Portion of the Muscular Coat of the Stomach, 37. A Portion of an Area in the Submucosa, Largely Composed of Groups of Cancer Cells, *. 38. Section of Tissue Near the Base of a Carcinomatous Ulcer, Showing Micro- organisms ( Colored ), 39. Diagrammatic Illustration of the Mechanism Effecting Vertical Position of the Stomach, . . . ' 40. Dilation of the Stomach, 105 116 117 1 1 7 121 123 124 129 140 142 143 169 179 183 299 300 303 303 3°7 309 3 IQ 3ii 452 473 474 528 529 531 532 628 6 3 s *» 1 TABLE OF CONTENTS. PART FIRST. ANATOMY AND PHYSIOLOGY OF THE DIGESTIVE ORGANS.- METHODS AND TECHNICS OF DIAGNOSIS. CHAPTER I. Page Anatomy of the Stomach, 17-24 Muscular Layer. — Structure of the Mucous Membrane. — Three Kinds of Cells of the Peptic Glands. CHAPTER II. Histology of the Stomach, 24-31 Mucosa. — Vessels and Nerves. CHAPTER III. The Small Intestine, 31-41 Structure. — Valvulte Conniventes. — Villi. — Lacteals. — Glands. — Blood-vessels. — Lymph-vessels. — Relations of the Duodenum. — Jeju- num and Ileum. CHAPTER IV. Physiology of Digestion, 41-48 Food Substances. — Caloric Values. — Ptyalin Digestion. — Digestion of Starches. — Gastric Juice. CHAPTER V. Pepsinogen and Pepsin. — Rennin Zymogen and Rennin. — Intestinal Digestion. — Duodenal Intubation, . . 49-58 Rennin, Chymosin, or Pexin. — Physiology of Intestinal Digestion. — The Pancreas : Its Secretion and Pancreatic Digestion. CHAPTER VI. The Bile. — The Succus Entericus. — Intestinal Fermen- tation. — Putrefaction. — Formed or Organized Ferments, 59-64 CHAPTER VII. Effects of the Action of the Several Digestive Secre- tions. — Methods for Testing the Motor Func- tions of the Stomach, . . 65-71 Qualitative and Quantitative Methods for Testing the Motor Functions of the Stomach. XV Xvi TABLE OF CONTENTS. CHAPTER VIII. Methods for Testing the Gastric Peristalsis, .... CHAPTER IX. Hemmeter’s Method for Testing the Gastric Peris- talsis, . Theories Concerning the Movements of the Ingesta. CHAPTER X. Absorption from the Stomach, Penzoldt’s and Faber’s, Herschel’s, Julius Miller’s, and Hemmeter’s Tests for Gastric Resorption. CHAPTER XI. Methods for Determining the Location, Size, and Capacity of the Stomach, Percussion and Auscultation. — Location, Size, and Capacity. — Gastro- diaphany of Einhorn. — Literature. CHAPTER XII. The Stomach-tube and Technics of Its Introduction, . . Examination of Stomach Contents. — Test-meals: Their Effect upon the Amount of Acid Secreted.— Literature. CHAPTER XIII. Methods for Qualitative and Quantitative Analysis of Stomach Contents, Presence of Bits of Gastric Mucosa. — Examination of Stomach Con- tents for Mucus, Saliva, Bile, Duodenal Secretions, Blood, and Pus. — Tests for Blood in Stomach Contents. — Demonstration of the Presence of Iron in Stomach Contents or Vomited Matter. — Spectroscopical Ex- amination of Stomach Contents for Blood. — Examination of Portions of Mucosa or Tissue Found in the Wash-water or Vomited Matter. — Character and Amount of Undigested Food. — Bacteria. — Literature. CHAPTER XIV. The Diagnostic Significance of Fragments of Gastric Mucosa, Deductions from Fifty Cases. CHAPTER XV. The Chemistry of Gastric Digestion, Occurrence of Secretions in the Empty Stomach. — Stimulations to Secretions of Gastric Juice. — Significance of Foam. — Preparation of Gastric Contents. — Quantitative Analysis. — Methods. — Standard or Normal Solutions. — Indicators. — Titration. — Apparatus. CHAPTER XVI. Chemical Examination of Gastric Juice, Tests for Presence of Free Acids. — Tests for Free Hydrochloric Acid. — The Dimethyl-amido-azo-benzol Test. — The Resorcin Test. — Com- bined Hydrochloric Acid. — Lactic Acid : Formation, Significance, Detection. — The Phloroglucid- Vanillin Test. Page 72-78 79-90 90-97 98-1x3 114—126 127-139 139-148 148-155 i 5 6 ~ i6 3 TABLE OF CONTENTS. Xvii CHAPTER XVII. Page Quantitative Analysis of the Stomach Acids, 163-171 Topfer’s Method. — Method of Martius and Lttttke. — Leo’s Method. — Boas’ Method. — Lactic Acid : Quantitative Estimation, Boas’ Method. — Quantitative Estimation of Fatty Acids. — Total Organic Acids. • CHAPTER XVIII. Digestive Ferments. — Products of Digestion. — Tests for Same, 171-177 Saliva. — Pepsin. — Pepsinogen. — Chymosin or Rennin and Rennin Zymogen. — Action of Pepsin on Proteids. CHAPTER XIX. Gastroscopy, 178-184 Description of the Instrument. PART SECOND. THERAPY AND MATERIA MED1CA OF STOMACH DISEASES. CHAPTER I. The Principles of Dietetic Treatment of Gastric Diseases, 185-227 Preparations of the Foods. — The Diet as Influenced by the State of the Secretion. — The Dietetics of Gastric Ulcer and Erosions. — The Indica- tions for Predigested Foods: Peptones, Albumoses, Dextrose, etc. — Rectal Alimentation. — The Occurrence of Proteolytic Ferments in the Colon and Rectal Contents. — Preparation of Rectal Enemata. — Indica- tions Necessitating Rectal Feeding. — Tables of Dietetics. CHAPTER II. Dietetic Kitchen. — Diet Lists, 228-287 Effects of Cooking on Food. — Indications of the Palate. — Dietetical Cooking. — The Use and Abuse of Rest and Exercise for the Digestive Organs. — Mental Rest. — Dietetic Exercise. CHAPTER III. The Dietetics of Alcohol and Alcoholic Beverages, . Action of Alcohol on Pancreatic Digestion. — Action of Alcohol on Salivary Digestion. — Action of Alcohol on Gastric Peristalsis. — Effect on Absorption. CHAPTER IV. Lavage and the Gastric Douche, The Gastric Douche. — Electricity in the Treatment of Gastric Diseases. — Hydrotherapeutic and Orthopedic Methods. — Gastric Massage. — Combination of Massage and Medicated Irrigations of Stomach and Colon. CHAPTER V. Mineral Springs, The Uses and Abuses of Natural Mineral Waters in Diseases of the Digestive Organs. — Useful Mineral Springs of the United States, with Analyses and Mode of Action. 287-297 297-313 3 1 3-3 2 8 XV 111 TABLE OF CONTENTS. CHAPTER VI. PAGE Important Medicinal Agents in Gastric Therapy, . . . 328-347 Hydrochloric Acid. — The Alkalies. — The Bitter Tonics and So-called Stomachic Remedies. — Digestive Ferments. CHAPTER VII. Surgical Treatment of Organic Gastric Diseases, . . 348-373 Various Forms of Operations Practised upon the Stomach. — The Fundamental Factors Influencing the Rate of Mortality in Gastric Operations. — Operative Statistics. CHAPTER VIII. Influence of Gastric Diseases upon Other Organs and on Metabolism, „ 374-400 The Influence of Diseases of Other Organs on the Stomach. — Literature. CHAPTER IX. The Blood and Urine in Stomach Diseases, 400-413 The Gases of the Stomach. — Urinary Changes in Stomach Diseases. PART THIRD. THE GASTRIC CLINIC. CHAPTER I. Acute Gastritis, 414-443 Simple Acute Gastritis. — Phlegmonous or Purulent Gastritis. — Suppur- ative Inflammation of the Gastric Mucosa. — Abscess of the Stomach. — Infectious Gastritis. — Gastritis Mycotica or Parasitaria. — Gastritis Diphtherica and Crouposa. — Toxic Gastritis. — Gastritis Venenata. CHAPTER II. Chronic Gastritis, 443-486 Literature. CHAPTER III. Ulcer of the Stomach, 486-526 Ulcus Ventriculi, Pepticum, Rotundum, Perforans, Rodens, Corrosivum, e Digestione. — Literature. CHAPTER IV. Malignant Tumors of the Stomach, 527-589 Carcinomata.— Sarcomata. — Literature. — Table of Differential Diag- TABLE OF CONTENTS. XIX CHAPTER V. PACK Stomach Diseases Caused by Infectious Granulomata, . 590-606 Tuberculosis of the Stomach. — Syphilis of the Stomach. — Literature. CHAPTER VI. Benign Tumors of the Stomach, 606-623 Myomata. — Fibromata. — Lipomata. — Polypi. — Myxomata. — Papillo- mata. — Lymphadenomata. — Pedunculate Tumors. — Foreign Bodies. — Gastroliths. — Hypertrophic Stenosis of the Pylorus. — Literature. CHAPTER VII. Motor Insufficiency, 624-682 Gastric Atony or Myasthenia. — Gastrectasis (Dilation of the Stom- ach). — Obstruction of the Orifices. — Literature. CHAPTER VIII. Hemorrhage from the Stomach (Gastrorrhagia), . . . 682-694 CHAPTER IX. Enteroptosis — Gastroptosis, 695-732 History and Pathogenesis of Enteroptosis. — Observation on Gastrop- tosis. — Observation on Dislocation of the Colon. — Observation on Dis- location of the Liver. — Literature. CHAPTER X. Neuroses of the Stomach, 733~794 General Considerations. — Cardiospasm. — Pyloric Spasm. — Gastro- spasm. — Gastric Hyperperistalsis. — Nervous Eructation. — Nervous, Habitual, or Reflex Vomiting. — Insufficiency or Incontinence of the Cardia. — Rumination, or Merycism. — Insufficiency or Incontinence of the Pylorus, — Atony of the Stomach. — Literature. CHAPTER XI. Sensory Neuroses, 794-816 Hyperesthesia. — Gastralgia. — Bulimia, or Hyperorexia. — Acoria. — Nervous Anorexia. CHAPTER XII. Neuroses of Secretion, 817-849 Hyperchylia. — Periodic Atypical Flow of Gastric Juice. — Chronic Continuous Flow of Gastric Juice. — Literature. — Subacidity. CHAPTER XIII. Achylia Gastrica, 850-864 CHAPTER XIV. Nervous Dyspepsia (Leube). — Neurasthenia Gastrica (Ewald), 865-876 Heterochylia. List of Authors, 879 List of Subjects, 889 Diseases of the Stomach. PART FIRST. ANATOMY AND PHYSIOLOGY OF THE DIGESTIVE ORGANS.— METHODS AND TECHNICS OF DIAGNOSIS. CHAPTER I. ANATOMY OF THE STOMACH. The organic diseases which affect the human stomach produce decided and characteristic changes in its structure. For the proper comprehension of these, a brief outline of the normal anatomy and histology is indispensable. Even a short reference to the embry- ology of the human stomach will have to be made, but this will be limited to the two diseases — viz., enteroptosis and gastroptosis, the pathogenesis of which will become more intelligible by a review of the fetal development of this organ. Many valuable contributions to the subject of the macroscopical and microscopical anatomy of the stomach have been made during recent years. In the subjoined brief synopsis we have availed ourselves of the valuable researches of F. Mall, and of the works quoted by him in the bibliography given in his article in the “ Johns Hopkins Hospital Reports,” volume I. The comprehensive works of Oppel, Spalteholz, and others which have appeared during i 896-’99, have also been consulted. The stomach is the dilated, sac-like portion of the digestive tract, between the esophagus and the small intestine. One can distinguish a lower convex arch, the greater curvature, which is directed toward the left and downward ; and an upper concave arch, the lesser curvature, which is directed toward the right and upward. The broad left end of the greater curvature is called the 2 17 ANATOMY OF THE STOMACH. fundus, the size of which varies according to age. Between the fundus and the lesser curvature is situated the cardia, being the continuation and funnel-shaped expansion of the esophagus. 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 structure of the epithelial lining. This zigzag line separates the cardia from the esophagus. At this point the arrangement of the muscular fibers and veins is also different from that in the esophagus. The location of the cardia in the adult is at the twelfth dorsal vertebra. At about the height of the bifurcation of the bronchi, the spiral curving of the esophagus around the aorta begins. By executing this curve, the convexity of which is toward the right, the esophagus gets to the left side of the aorta, and passes through the diaphragm in the foramen cesophageum, near the spinal column. The stomach becomes narrower from the fundus toward 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 mucous membrane, the latter forming the pyloric valve, the opening of which is of varying diameter. The part of the stomach in advance of the pylorus is called the pyloric antrum, and is frequently separated from the greater curvature by an inden- tation or depression. This antrum may be elongated so as to assume resemblance to the intestine ; this is more frequently the case in the female. On the anterior and posterior walls of the stomach, running along between the muscular and serous coats of the organ, are two band-like stripes, consisting of elastic, smooth, muscular fibers, — the pyloric ligaments. The size of the stomach depends upon age, sex, and individuality, and upon the degree of its distention. The long axis varies from 25 to 35 cm. The greatest vertical measurement, at the cardia, is 15 cm., and the greatest straight diameter is from 11 to 12 cm.; the smallest, at the pyloric antrum, is from 3 to 4 cm. In the female it is generally smaller and more slender. The capacity varies considerably: Ewald considers from 1600 to 1700 c.c. to be the normal limit. Three-fourths of the stomach belongs to the left half of the body and one-fourth to the right half. The cardia is located behind the median edges of the fifth DIAPHRAGM — PANCREAS. >9 and sixth ribs. The fundus, the largest part of the body of the organ , is in the left hypochondrium ; the rest, with the pyloric part, is in the epigastrium. 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 ensiform cartilage. The lesser curvature runs along to the left, and near 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 half of an imagi- nary straight line connecting the ensiform cartilage with the umbili- cus. Both the highest and lowest parts of the stomach are moved about according to the level of the diaphragm and the distention of the stomach. In an empty condition, the stomach is withdrawn into the upper portion of the abdomen ; but when filled, it distends in all directions, but mostly in the direction of its long axis, from the left above, downward, and to the right. In a state of moderate distention about forty centimeters 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 left segment, while the left lobe of the liver, up to the sulcus inter- lobularis, covers the smallest part — that is, the lesser curvature and the pyloric portion. From this fact arises the difficulty in palpating tumors in the latter places, which is impossible except when gastroptosis, or 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 can not change its location to any considerable extent, and the change of location of the whole stomach caused by filling is produced almost exclu- sively by an extension of the greater curvature. The pancreas extends along the posterior wall of the stomach. At the upper edge of the pancreas are the splenic artery and vein. The transverse colon runs along the greater curvature, and its left flexure fills the remaining space in the left hypochondrium. The location of the stomach is fixed by a ligamentous attachment of the cardia, by 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 the author have proved that intra-abdominal pressure adds nothing to the support of the stomach. The gastrophrenic ligament, which toward the right passes into the lesser omentum, and toward the 20 ANATOMY OF THE STOMACH. left extends into the phrenosplenic ligament, surrounds and em- braces the cardia. This portion is lower than the fundus, its situation corresponding 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 therefore 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 vertebrae ; 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 transverse mesocolon. This is the reason why changes of location in the greater omentum (hernia and inflammatory adhesions) can produce traction upon the stomach. As the stomach is really attached only at the cardia, and the pylorus is adherent to the posterior abdominal wall, together with the descending portion of the duodenum, the organ is capable of being moved about, not so much in its entirety as in its parts (the great curvature, for instance). The stomach has a complete peri- toneal covering which consists of an anterior and a posterior layer, uniting at the two curvatures of the stomach to form the lesser and the greater omentum ; between these two layers space is left for the blood- and lymph-vessels of the stomach. Muscular Layer. — The muscular stratum contains three kinds of fibers — longitudinal, transverse, and oblique. The longitudinal layer of muscular fibers — a continuation of those of the esophagus — presents a denser arrangement at the lesser curvature than at the greater, and forms the ligamenta 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 it crosses at right angles. The circular fibers run around the stomach in a ring or belt-like manner; at the pylorus they form a local thickening of the muscle rings — the pyloric sphincter. A fold of the mucosa to the innermost side of this sphincter constitutes the pyloric valve. The longi- tudinal fibers also have a part in the formation of the sphincter, for while the superficial layer of longitudinal fibers passes on over the pyloric sphincter into the duodenum, the deeper longi- tudinal fibers enter the pyloric valve, encircling and grasping the circular fibers in a loop-like manner (dilator pylori — Rudinger). The cardia has no special sphincter, but the oblique fibers cross and decussate at the periphery of this portion. The sphincter MUCOUS MEM B KANE. 2 I pylori is contracted during digestion, but 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, uniform layer, some passing obliquely from left to right, others from right to left, around the cardiac orifice. The sub- mucosa, or cellular coat of the stomach, consists of a loose, fila- mentous, areolar tissue, and loosely binds the mucosa to the muscular layers. The most important and interesting layer is the mucosa, or mucous membrane proper of the stomach. It is a thick layer with a smooth, soft, velvety surface. During infancy and immediately after death it is of a pinkish tinge, but in adult life and in old age it becomes of a pale straw or ash-gray 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, have a longitudinal direction, and are most marked toward the lesser end of the stomach and along the greater curva- ture ; 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 pecu- liar honeycomb appearance, from being covered with small, shallow depressions, or alveoli, of a polygonal or hexagonal form, which vary from to 3-^- of an inch in diameter, and are separated by slight ridges. In the bottom of the alveoli are seen the orifices of minute tubes, — the gastric follicles, — which are situated perpendicularly side by side in the entire substance of the mucous membrane. They are short and of a simple tubular character toward the cardia, but at the pyloric end they are longer, more thickly set, convoluted, and terminate in dilated saccular ex- tremities, or are subdivided into from two to sixteen tubular branches. Watney has pointed out that these convoluted or coiled tubes form the transition from the simple tubular follicles to the convo- luted glands of Brunner, which lie immediately below the pylorus. Some histologists speak of a homogeneous basement membrane, formed by the connective-tissue framework, lined upon its free sur- face by a layer of cells, which differ in their character in different parts of the stomach. The author could never confirm the existence of such a basement membrane. Toward the pylorus the tubes are lined throughout by columnar or cuboidal epithelium ; they 22 ANATOMY OF THE STOMACH. are termed the mucous glands, and are supposed to secrete the gastric mucus. In other parts of the organ the deep part of each tube is filled with nucleated cells, the upper fourth of the tube being lined by columnar epithelium : these are called the peptic glands, and are the source of the gastric juice. Simple follicles are found in greater or less numbers 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 of the mucous membrane of the stomach and its alveoli is of the columnar variety. Usually four to sixteen 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 spread out upon a flat surface (Hyrtl and Luschka). The gland tubules are as long as the entire thickness of the mucosa, and their sac-like and branched bases extend into the muscularis mucosae, the contraction of which assists in the evacuation of the tubules during digestion. The ends of the tubules extending into the muscular layer are usually branched. Three Kinds of Cells of the Peptic Glands. — First, the cylin- drical cells of the gland duct and pit, lining one-fourth to one- third of the distance from the surface of the mucous membrane downward. They are a continuation of the cylindrical epithelium of the general internal surface of the gastric mucous membrane, apparently secreting mucus only. Secondly, the lightly colored pyramidal or cuboidal cells, with a granular protoplasm and spherical nucleus. These cells do not stain with anilin, 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 transparent during fasting, and become cloudy and granular during digestion. Heidenhain designated them as the chief or central cells, and they were held by him to be the sources of the ferments pepsinogen and rennin zymogen. These chief or central cells touch the lumen of the duct more extensively than the following variety. The third kind of peptic cells are known as the border, parietal, or oxyntic cells; they rest upon the connective-tissue framework with much broader bases than the chief or central cells. For this very reason they participate to a less degree in the limitation of the lumen of the duct. They are generally round or triangular, finely granular, PEPTIC CELLS. 23 and stain intensely with anilin, and were designated by Rollet as deloniorphous cells. Heidenhain supposes them to be the sources of hydrochloric 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 ( a ) the fundus of the gland tubule ; then ( b ) the outer secretory por- tion ; (c) the inner secretory portion ; and, opening on the inner surface of the mucosa, (d) the alveolus (“ Vorraum ”). Then, one finds the border, parietal, oxyntic, deloniorphous, or anilin cells most numerous in the outer secreting portion, and becoming scarce in the fundus or end portion. A fourth kind of cell, occurring at rare intervals, is known as Nussbaum’s cell; its significance is unknown. Heidenhain asserted that there were no border cells in the fundus at all ; but this has been denied by Stohr, Kupffer, and Boas. The size of border or acid cells depends upon the stage of diges- tion ; as this function proceeds, the border cells increase, and diminish again at the end of digestion. The chief, central, or fer- ment cells enlarge also, and become darker during digestion. In a fasting state the chief cells are largely in excess. Heiden- hain’s conclusions, that the chief or central cells are producers of the digestive ferments, and that the border or anilin-staining cells produce the hydrochloric acid, have been confirmed by a number of other observers (Griitzner, von Swiezicki, and, recently, Sehr- wald and Mall). It is known that the glandular tubules of the pyloric region con- tain only chief or central cells (producing ferments only, and no acid), while the gland tubules of the fundus contain both central cells and also border or acid cells. Heidenhain succeeded in re- moving the pyloric portion of the stomach entirely in a number of dogs, and uniting the organ with the external abdominal wall. In other dogs he removed the fundus entirely, leaving the pyloric portion intact, and succeeded in making this altered stomach with- out a fundus unite with the external abdominal wall. 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 con- tained both acid and pepsin ; these are therefore produced by the glands of the fundus which contain both varieties of secretory cells. In the animals that had been deprived of the fundus by ex- cision, however, the only secretory surface that was left being the 24 HISTOLOGY OF THE STOMACH. pyloric region, it was found that an alkaline juice was secreted con- taining only ferments. That this juice did contain pepsin was proved 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, which do not stain with anilin, the conclusion seems justifiable that the chief cells secrete only ferments, and that there- fore the border or anilin-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 tiny canaliculi — extensions from the central lumen of the gland to, or into, the oxyntic or acid cells. These canaliculi were brought out with the silver stain by Golgi. CHAPTER II. HISTOLOGY OF THE STOMACH. R. R. Bensley, B.A , M.B., has published a very interesting paper on the “ Histology and Physiology of the Gastric Glands,” in the “ Proceedings of the Canadian Institute,” 1896. The work was done in the biological laboratory of the University of Toronto. Mr. Bensley was kind enough to present us with four sketches illustrating the various phases of secretion in the gland cells of the deep ends of the fundus glands of the cat’s stomach. We consider his results a valuable addition to the work of Heidenhain, Ebstein, Langley, Sewall, and others. We have, by repeating his methods, assured ourselves that with staining as used by him, it is possible to recognize the precursory stages of the ferments within the structure of the cells. We submit the drawings, with explana- tory text. The following are his conclusions : “ 1. During digestion, a substance similar in chemical properties to the chromatin of the nucleus makes its appearance in the outer clear zone of the chief cells of the fundus glands. This substance, which may be called prozymogen, stains deeply and readily in hematoxylin, and presents a characteristic fibrillated appearance. During rest this prozymogen is used up in some way, giving rise to zymogen granules. MUCOSA. “ 2. The chief cells of the neck of the glands do not contain at any period of digestion either zymogen or prozymogen, but are engaged in the formation of a mucinoid secretion, which has a powerful elective affinity for indulin and Bordeaux red, and stains metachromatically in thionin. “ 3. The pyloric gland cells, likewise, form neither zymogen nor prozymogen, and are similar in structure, in staining properties, and in the nature of their secretion, to the cells of the neck of the fundus gland. “ 4. The cells of the pyloric glands and of the neck of the fundus glands pass, by gradual transition, into the mucous cells of the surface, to which they are obviously closely allied.” From Mall’s article on the anatomy of the stomach (“Johns Hopkins Hospital Reports,” vol. 1) we have quoted the following graphic description : Mucosa. — That more than one kind of gland is present in the stomach has been repeatedly noticed (Wassman, Frerichs, Brinton, Leydig, Kolliker), but a more careful study of them was delayed until 1870 (Heidenhain, Rollet). There are two kinds of glands present in the dog’s stomach — the pyloric and the peptic. The peptic, in turn, are formed in great part of two kinds of cells — the border or oxyntic and the central or ferment cells. A study of descriptions of Mall and Oppel shows that in the pyloric region the necks of the glands are the longest (0.68 mm.), and that they diminish in length throughout the middle zone (0.25 mm.), until the cardiac portion is reached. In the pyloric por- tion, where the necks of the glands are the longest, many gland tubes empty into one outlet; in the middle zone there are less, in rough about nine, into each gland mouth ; while in the cardiac por- tion each gland has a special opening — in other words, there are no gland necks. In the pyloric portion the glands are composed wholly of central cells. In the central zone there are many border cells, the proportion to the central cells being as described by Heidenhain and his pupils. Throughout the fundus are but few border cells, while around the esophagus there is a small zone in which there are many border cells. According to Mall, about 1600 gland tubes open within each square centimeter of mucous membrane in the pyloric portion, in the middle zone 2500, and in the fundus 4900. For an average stomach there is an area of about 28 square cm. in the pylorus, 108 in 26 HISTOLOGY OF THE STOMACH. the middle zone, and 120 in the cardiac portion, or these surfaces are to each other as 7 : 27 : 30. The estimation carried further gives somewhat over 1,000,000 gland openings in the stomach. Fig. 3. Sections ok Deep Ends of Fundus Glands of the Cat in Different Secretive Phases. X 1000 — {Bens ley.) Fig. i. — From a fasting stomach. The chief cells are filled with large zymogen granules; nuclei near the outer ends of cells. Gentian-violet preparation, b. Border cells. Fig. 2.— Six hours after an abundant meal of raw flesh. The chief cells exhibit two zones, the inner occupied by large zymogen granules, the outer by a deeply staining, obscurely fibrillar element, prozymogen ; the nuclei lie at the junction of the two zones, b. Border cells, pr. Pro- zymogen. c. Mucin secreting cell, similar to those found in the neck of the gland. Gentian- violet preparation. Fig. 3. — Twelve hours after feeding with sponge soaked in fat. Preparation stained in hema- toxylin exhibits a deeply stained outer zone filled with prozymogen, and a clear inner zone from which the granules have disappeared in course of preparation. The nuclei are now much nearer to the lumen, b. Border cells, pr. Prozymogen. On the other hand, if the blind tubes opposite the muscularis mucosae are estimated, the number exceeds 16,500,000. In other words, each gland neck subdivides sixteen times, on an average, MUCOSA. 2 7 before the muscularis mucosae is reached. It may be interesting to note that for each gland opening in the stomach we have one villus in the intestine, and for each subdivision there is one Lieber- kiihn’s crypt. The observations quoted, as well as those of others, apparently do not confirm Heidenhain’s statement — i. e., that “ wherever we have central cells we have pepsin.” Yet it seems true that the degree of acidity is in proportion to the number of border cells present in any portion of the stomach, and that there are portions of the stomach which do not contain border cells, but yield pepsin. In general, the formation of pepsin is most marked in those por- tions of the stomach which produce most acid ; and this ought to be the case, for acid favors the formation of pepsin from pepsino- gen (Podwyssozki, Langley, and Edkins), and the pepsin seems more or less combined with acid (Schiff, Richet). We must, there- fore, conclude with Heidenhain that the border cells play a most important part in the formation of acid. Between the glands lie the blood-vessels, lymphatics, some round cells, and the reticulum. In those portions of the stomach in which there is a “ neck zone,” there is a distinct layer of reticulum fibrils. In this layer peculiar spindle cells are frequently seen which surround the gland openings and appear much like the subepithelial cells in the villi of the intestine. Under no condition could a basement membrane be isolated, nor does Mall believe it exists, but instead there is a most beautiful network of the reticulum. “ Conclusions. — From a histological standpoint the mucous membrane of the stomach may be divided into three zones — the pyloric, with no border cells; the middle, with many border cells; and the fundus, with but few border cells. “ Digestion of the different portions of the mucous membrane with weak HCi shows that the middle zone digests most easily, the fundus less quickly, and the pyloric, as a rule, not at all. Assum- ing that the rapidity of digestion of the different portions is in proportion to the quantity of pepsin present, it makes it probable that most pepsin is formed in the middle zone. Although it has been proved that pepsin is formed in glands which do not contain border cells, in general it may be stated that the amount of pepsin formed by the different glands is in proportion to the number of border cells. “ The degree of acidity of the mucous membrane is in proportion to the number of border cells present. It is reasonable to suppose 28 HISTOLOGY OF THE STOMACH. that the formation of acid in any portion of the stomach aids materially in the formation of pepsin in the same part. This is very essential, because acid favors the formation of pepsin from pepsinogen. Since border cells are only with the greatest diffi- culty digested in acid, we can not ascribe to them the power to secrete pepsin ; and since the morphology of the central cells varies during digestion and rest, and they are so easily digested upon the addition of acid, we must conclude with Heidenhain that the former are probably concerned in the production of acid and the latter in the production of pepsin. “ When the stomach is forcibly distended, it is found that the dilatation is mostly at the expense of the fundus. This seems also to be the case when the stomach is naturally filled with food. Although the middle zone is practically not stretched when the stomach is filled, distention seems to favor circulation through this part because the blood-vessels are more easily injected in a moder- ately distended, than in an empty, stomach. “ In the intestine it is found that the longitudinal and circular muscle-fibers are antagonistic. In the stomach the pyloric valve is closed, after the muscle-cells are dead, by a fold of mucous mem- brane being thrown into the lumen. This may take place in a living stomach. A contraction of the circular muscle tends to strengthen this valve, while a contraction of the longitudinal muscle tends to weaken it, because with the contraction of the longitudinal muscle there is always an accompanying relaxation of the circular muscle. Under ordinary circumstances it seems as though the stomach reduced its lumen by simultaneous contraction of both longitudinal and circular muscle-fibers. What complex motions take place during peristalsis are absolutely unknown. It is, how- ever, a remarkable fact that a bundle of the circular fibers (oblique fibers) are parallel with the longitudinal fibers, which are increased in number in the middle zone. A solution of this problem seems within the range of experimentation. “ The celiac axis supplies, besides the stomach, also the spleen and the liver. With a given pressure within the aorta, variation in the resistance in the capillaries of the spleen and the liver will have a marked effect upon the circulation through the stomach. The portion of the stomach (middle zone) supplied by the gastric artery is to a less extent under the control of these side influences than is that which is supplied by arteries arising from the main branches to the spleen and to the liver. It must be again stated that there Three Sections of Stomach-walls Placed Side by Side to Show the Positions of Blood-vessels and Lymphatics to the Different Layers. — (F. Mall , “ Johns Hopkins Hospital Reports Vol. I.) M. Mucosa. M ' . Muscularis mucosae. S. Submucosa. C and Z. Circular and longitudinal muscles enlarged 70 times. PLATE 11. LIBRARY OF THE UNWERSITY of ILLINOIS. MUCOSA. 29 are, in all probability, many other influences which play most im- portant parts in the distribution of blood. “ 7. Around the two curvatures of the stomach there is a com- plete circle of anastomosis, which has a tendency to equalize the pressure in the arteries penetrating the muscle-walls. But the anastomoses arising therefrom have only a tendency to make gradual gradations, and not an equal pressure throughout. The additional set of anastomoses within the submucosa are, again, not sufficient to equalize the flow throughout the whole mucosa. After ligating arteries, as well as by examining the mucous mem- brane, during digestion and rest, it is found that no sharp lines can be drawn. “ 8. The blood-vessels are arranged in such a manner that from any portion of the submucosa about one-fourth of the blood may go to the muscle-coats and three-fourths to the mucosa. It is therefore probable that when the flow is poured to one side it is diminished to the other, and vice versa. There is, however, a ten- dency to equalize this by the submucous anastomoses. “ 9. Since there is but one set of arteries to the mucosa, there must be but one sort of circulation, which may vary in degree only. Within the mucosa the arrangement is such that the portion of the gland which is deepest receives the blood richest in O. The mucous membrane, omitting the muscularis mucosae, lies between two venous plexuses. Contraction of the muscle-fibers between the glands and those of the muscularis mucosae should diminish the volume of the mucosa. This would have a tendency to empty the glands, as well as to press blood from the two venous plexuses, especially the lower. Whether or not there is a force within the mucosa which can augment the circulation seems at present im- possible to determine by experiment. The arrangement of the parts is very suggestive. “ 10. The rich venous plexus of veins within the submucosa is sufficiently large to hold a considerable quantity of blood. This must be the case when the valves within the veins coming from the stomach are temporarily closed. When the valves are closed, a contraction of the circular muscle is sufficient to drive all the blood from the underlying veins. It is therefore possible that a rhythmical contraction in any part of the stomach may favor the circulation through its walls. “ 1 1 . The arrangement of the lymphatics is much the same as that of the veins, and the foregoing consideration (10) applies equally 3 30 HISTOLOGY OF THE STOMACH. well to them. When we consider the resistance to be overcome while the lymph passes through so many networks before the cis- terna chyli is reached, it makes it plausible to state that the circu- lation is favored by muscular contraction. “ 12. Since the blood which leaves the stomach must pass through the capillaries of the liver, it is necessary that it be con- stantly under a comparatively high pressure. This pressure is also dependent upon the spleen and the intestine. If the pressure is high, a regurgitation into the stomach is impossible on account of the presence of valves. “ 13. In a stomach in which the vessels are all equally distended the rapidity of circulation in the celiac axis would be 263 times that in the capillaries. The area of the section of the celiac axis is 0.0592 square cm. ; the immediate branches to the stomach, 0.0348 square cm. ; to the spleen and liver, 0.0244 square cm. All the capillaries of the stomach: mucosa, 6.4524 square cm. ; muscle- coats, 2.7214 square cm.; total, 9.1738 square cm.; 9.1738 0.0348 = 263. “ A like estimation shows that the rapidity of circulation in all the capillaries is ^3 of that in the arteries penetrating the muscle- walls ; while if the capillaries of the muscle-walls are excluded, the rapidity in the capillaries of the mucosa rises to “ Considering the glands on an average 0.05 cm. long and 0.003^ cm. in diameter, excluding the necks, the area of all the glands would be 8671 square cm., or thirty-eight times the area of mucous membrane. A like estimation of the capillaries, considering each capillary 0.04 cm. long, gives for them a total area of 1718 square cm., or 7J/2 times the mucous surface. The secreting surface is five times that of the blood-supply.” Vessels and Nerves. — The arteries supplying the stomach are: the coronaria ventriculi ; the pyloric and right gastro-epiploic branches of the hepatic ; the left gastro-epiploic and vasa brevia from the splenic. They supply the muscular coat, ramify in the submucous coat, and are finally distributed to the mucous mem- brane. The arrangement of the vessels in the mucous membrane is somewhat peculiar. The arteries break up at the base of the gastric tubules into a plexus of fine capillaries which run upward between the tubules, anastomosing with one another and ending in a plexus of large capillaries which surround the mouths of the tubes, and also form hexagonal meshes around the alveoli. (See Plate II.) The veins arise from the latter, and pursue a straight THE SMALL INTESTINE. 3 I course back to the submucous tissue, between the tubules, to terminate in the splenic and portal veins. The lymphatics are abundant, and may be divided into a super- ficial and a 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. (Solar plexus.) CHAPTER III. 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 twenty-two feet in length in an adult, and becomes gradually narrower from its upper to its lower end. Its convolu- tions occupy the middle and lower parts of the abdomen, fre- quently descending into the pelvis. The small intestine is divided into three portions, which have re- ceived different names : The first ten to twelve inches immediately succeeding the stomach, and comprising the widest and most fixed part of the tube, are 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 de- marcation between the jejunum and the ileum, yet that portion of the small intestine included under these two names gradually un- dergoes certain changes in structure and appearance from above downward, so that the upper end of the jejunum can readily be dis- tinguished from the lower end of the ileum. Structure of the Small Intestine. — The small intestine, like the stomach, is composed of four coats — viz. : the serous or peri- toneal, the muscular, the areolar, and the mucous. The external, or serous, coat almost entirely surrounds the intes- 32 THE SMALL INTESTINE. tinal tube in the whole extent of jejunum and ileum, leaving only a narrow interval behind, where it passes off and becomes continuous 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 consists of two layers of fibers — an outer longitudinal, arid 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 toward 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 onward through the canal. In the narrowing of the tube the circular fibers are mainly concerned, the longitudinal fibers 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 plexus of nerve-fibers and a network of lymphatic vessels betweeen 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 it contains a gangliated plexus of nerve-fibers and a network of large lymphatic vessels. The internal coat, or mucous membrane, is characterized by the * finely flocculent, or shaggy appearance of its inner surface, resem- bling 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 vascufar 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, toward the lower end. It is lined with columnar epithelium throughout its whole extent, and, next to the submucous coat, is bounded by a layer of plain muscular tissue (muscularis mucosae) ; between this and the epithelium the substance of the membrane, apart from the tubular glands, which will be after- ward described, consists mainly of retiform tissue, which supports VALVUL/E CONNIVENTES. 33 the blood-vessels, nerves, lymphatics, and lacteals, and incloses in its meshes numerous lymph-corpuscles. Valvulse Conniventes. — The mucous membrane, in addition to small efifaceable folds, or rugae, possesses also permanent folds, which can not be obliterated, even when the tube is forcibly dis- tended. These permanent folds are the valvulae conniventes, or valves of Kerkring. They are crescentic projections of the mucous membrane, placed transversely to the axis of the bowel, and follow- ing one another closely. The majority 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 lumen of the bowel, but in rare cases may go around two or three times. At their highest point they project inward for about of an inch. Some of the valvulae con- niventes are bifurcated at one or both ends, and others terminate abruptly. Each consists of a fold of mucous membrane — that is, of two layers placed back to back, and united by submucous areolar tissue. They contain no part of the circular or longitudinal mus- cular coats. Being extensions of the mucous membrane, they serve to increase the absorbent surface to which the food is exposed. The valvulse conniventes are not uniformly distributed over the various parts of the small intestine. There are none just at the commencement of the duodenum : a short distance from the pylorus they begin to appear ; beyond the point at which the bile and pan- creatic juice are poured into the duodenum they are very large, regularly crescentic in form, and placed so near to one another 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 further apart, and, finally, toward the middle or lower end of the ileum, having gradually become more irregular and distinct, sometimes even acquiring a very oblique direction, they disappear altogether. The villi, peculiar to the small intestine, and giving to its inter- nal surface 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. 34 THE SMALL INTESTINE. They are largest and most numerous in the duodenum and jeju- num, and become 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 downward, 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 at their bases. In the upper part of the small intestine there are from io to 18 villi in a square millimeter, and in the ileum from 8 to 14 in the same space. This would give about 4,000,000 altogether (Krause). A villus consists of a prolongation of the mucous membrane proper. It is covered by columnar epithelium, and incloses a net- work of blood-vessels, one or more lymphatic vessels (lacteals), and a few longitudinal, plain, muscular fiber-cells, these being all sup- ported 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 throughout 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 base of the villus, and then up the center to near the middle line of the villus, where it begins to break up into a number of capillaries. These form, near the surface, a fine capillary network beneath the epithelium and limiting membrane, 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 center 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 forming the basement membrane ; from the latter, pro- longations extend between the epithelial cells toward the surface. THE VILLI. 35 Briicke first discovered the muscular tissue within the villus, con- sisting of unstriated, plain fiber-cells, disposed longitudinally around the lacteal. These fibers are prolongations of the muscularis mucosae. When they are stimulated in animals, a very evident retraction of the villus is observable. The fiber-cells at the sides and toward 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 is a variable number of leukocytes, 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 epi- thelial 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 stain readily with eosin. Hence he calls these cells eosinophilic. Among the ordinary epithelial cells of the villus are others, the outer half of which is filled with mucigen, and at times beaker- or cup-shaped empty cells are observed from which this has been discharged as mucus, the free end being ruptured; these are sometimes called the goblet-cells. The number of cells containing mucus varies much in different animals and under different condi- tions in the same animal. There are comparatively few mucous cells 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 interior 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 by whose gastric juice it has been formed, acts as a poison. It is due to these epithelial cells of the intestine that peptone is so modified 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 followed out to some extent. The 36 THE SMALL INTESTINE. examination of such specimens, taken during digestion of a meal containing fat, shows the epithelial cells turbid with oil droplets in their interior; and in some animals, at a subsequent stage, ameboid 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 ameboid lymph-corpus- cles, appearing so abundantly within the villus and among the epi- thelial cells on its surface, play an important part in the transfer- ence of such particles from the epithelial cells in the lacteal ; for at certain stages of fat absorption they contain abundant fatty par- ticles. Recent investigations point to the absorption of the larger portion of fats in form of fatty acids and soaps. The present state of our knowledge on the subject of the emulsion and solution theories of fat-absorption is, in the author’s opinion, by no means sufficiently matured to justify a scientific conclusion in favor of either hypothesis to the exclusion of the other. 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 ameboid cells, we have an analogous process. Glands. — Two kinds of true secreting glands are found in the intestine ; these are : (i) the glands or crypts of Lieberkiihn and (2) the glands of Brunner. In addition to these, there are found also two varieties of intestinal lymph-follicles, (1) the 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 Lieberkuhn’s glands, they are nevertheless spoken of as glands. The follicles, crypts, or glands of Lieberkiihn are tubular pits lined by columnar epithelium, occurring between the villi. 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 mucosa, their ends approaching the muscularis mucosse. The duodenum possesses an additional layer of true secreting structures in the glands of Brunner. They would appear to rep- resent the direct continuations and higher specializations of the pyloric glands. In passing from the stomach into the intestines, these tubules undergo repeated division, at the same time sinking THE BLOOD-VESSELS OF THE INTESTINES. 37 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 Lieberkuhn, which are con- tained in the mucosa proper. Brunner’s glands belong to the race- mose 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 Lieberkuhn crypts or sometimes into their bases. The solitary glands are isolated lymph-follicles scattered through the entire intestine, most abundant in the lower ileum. Situated in the mucosa, at times in the submucosa, the lymphoid tissue in them is 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 aggre- gations of lymph-follicles held together by diffuse adenoid tissue, limited to the lower two-thirds of the small intestine. Develop- ment of these is most perfect in the ileum ; appearing first within 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 is indi- cated by an elevation corresponding to them on the mucous sur- face. 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, giving 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, and then extending beneath the epithe- lium and around the central lacteals as far as the ends of the villi. These capillaries terminate in venous stems which descend almost 38 THE SMALL INTESTINE. perpendicularly 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 sub- mucosa 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 one-third of the total amount of blood of the body. The arteries are all branches of the superior and inferior mesen- teric arteries, which run along and approach the gut in the mesen- tery. The intestinal veins form the principal portion of the portal system. Lymph-vessels. — The beginning of the lymph-vessels can be traced to the lacteals within the villi, where they begin as tiny, blind pouches at the apex of the villus. In some broad villi there are two such lymph-vessels that anastomose with each other. From here they run down in the septa between the glands in the lymph-vessel meshwork over the muscularis mucosae. Here they again anastomose with an outer lymph-vessel network in the submucosa. Here 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 celiac plexus, the semilunar ganglion, and vagus nerve, consisting of medullated and non-medullated 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 numerous micro- scopical ganglia, constituting 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, villi, and limiting membrane. Relations of the Duodenum. — This part of the gut in the adult is horseshoe-shaped, generally presenting well-marked angles, which divide it into four parts having four distinct directions; these are: (i) The horizontal or superior part, running backward from the pylorus, to the right, in contact with the quadrate lobe of the liver, to the under side of the neck of the gall-bladder, where it curves sharply downward to join the second part. This first or horizontal part is about two inches long when the stomach is RELATIONS OF THE DUODENUM. 39 empty. (2) The second or descending portion is about three inches long, and commences just below the neck of the gall-bladder oppo- site the right side of the first lumbar veretebra, and passes down to the level of the third or fourth lumbar vertebra, where it turns sharply inward to join the third part. (3) The third or transverse portion is from two to three inches 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 upward to join the terminal, (4) fourth, or ascend- A Fig. 4.— Plaster Casts of Duodenum of Infant and Adult.— {From Museum of Harvard University .) A. Infant duodenum. B. Adult. V. Valvulae conniventes. P. Pylorus. 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 lumbar vertebra ; here it turns abruptly forward to join the jeju- num, 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 water-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, at the same time 40 THE SMALL INTESTINE. preventing the regurgitation of gases from the jejunum into the pyloric part of the duodenum and stomach. Jejunum and Ileum. — The upper two-fifths of the remaining intestine immediately following the duodenum are called the jejunum ; the lower three-fifths, the ileum. Both are attached to the posterior abdominal wall by an extensive fold of peritoneum, — 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 cecum, the colon, and the rectum. The colon is subdivided, according to the directions it takes, into four parts, which are (i) the ascending, (2) transverse, (3) descending, and (4) sigmoid colon or flexure. The end of the ileum, which rises out of the pelvis to the right iliac 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 cecum. From the inner and back part of the cecum, 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 cecum 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, and 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 hepatocolic and gastrocolic liga- ments respectively. The descending colon continues into the sigmoid colon or flexure, which connects it with the rectum. The rectum, following the curves of the sacroiliac symphysis and the hollow of the sacrum, has itself two curves : an upper larger curve, concave anteriorly, and a lower smaller curve, convex anteriorly. Only the cecum, transverse colon, and sigmoid colon have a com- plete peritoneal covering ; the rest of the large gut is only covered anteriorly. From the third sacral vertebra on, the rectum has no peritoneum. Those parts having no complete peritoneum, therefore, have no mesentery, and are not very movable. The longitudinal fibers are contracted, or narrowed down to three parallel bands (Fasciae teniae, or ligamenta coli). One of these bands runs along FOOD SUBSTANCES. 41 the attachment of the gastrocolic 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 longi- tudinal bands being shorter than the other layers of the wall of the colon, they bring about 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 in- voluntary fibers. The external sphincter is composed of striated voluntary muscle- fibers. The histology of the large intestine differs from that of the small by the absence of the villi and the 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 epithelium ceases to exist and flat pavement epithelium takes its place. CHAPTER IV. PHYSIOLOGY OF DIGESTION. Food Substances. — 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 compounds from them. It is compelled to take in these com- pounds in the form of proteid or albuminous substances, carbohy- drates, and fats, together with such inorganic bodies as water and salts. .Even these food-stuffs, which are essential for the maintenance and development 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 kingdoms. The innutritious admixtures of the food substances are not harmful, but are important as stimulants to the intestinal mucosa and to the evacuation of feces. Among these innutritious sub- stances are classed the connective tissue, cartilages and tendons of meat, and the cellulose of plants. 42 PHYSIOLOGY OF DIGESTION. Water plays a most important role in the economy of the body, for it goes to make up sixty per cent, of the total organism. We lose about 2 y 2 liters of water in twenty-four hours, through insensible perspiration, secretion, and defecation. About 300-400 gm. of water are formed by oxidations of food substances in twenty-four hours; so we have a deficit of 1500-1600 gm., which must be supplied by the daily consumption of a corresponding amount of water; this is done principally by the drinking of water after we have taken in part of it by our foods, or in the shape of beverages (soups, milk, fruits, vegetables, potatoes, beer, wine, coffee, tea, etc.). In mineral substances we must supply the daily loss of sodium chlorid 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 for the building up of the organism, and the continuance of life pro- cesses. The latter are the prevailing sources of heat and force; in the process of oxidation they finally reach the stages of H 2 C 0 3 and H 2 0 . In addition to these, a number of other substances occur in the food that are oxidized, 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, such as creatin in meat, glucosids, alkaloids, and ethereal oils in vegetables and spices, pass through the body without being oxidized or assimilated ; they are not foods, as they do not enter the metabolism of the body, nor do they develop energy by chemical transformation. However, a number of these are of importance in nutrition, as they render the food more palat- able, and stimulate the secretions and the motility of the digestive tract. It has been 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 are of some significance in the construction of tissue, although the organism can derive no energy from them, as they are always taken in a highly oxidized state, and leave in CALORIC VALUES. 43 the same condition. Nevertheless, the body will suffer if any one of these elements be excluded from the food. A certain minimum of these elements — the amount has not yet been ascertained — is absolutely necessary. Outside of the sub- stances named, the food contains, as previously stated, a number of materials that are not at all absorbable or digestible, and leave the digestive tract in an unchanged form ; this is the slag and dross of the food, and is taken into the body principally with vegetables. The normal adult human organism daily loses by its metabo- lism 120 gm. of albuminous or proteid bodies, 80 gm. fat, 400 gm. carbohydrates, 25 gm. salts, and 2 y 2 liters of water. Accordingly, a corresponding amount of food-stuffs must be introduced in the diet. The articles of food contain these nutritious substances in a variety of proportions. The rational combination of these sub- stances is one of the objects of dietetics. Gilman Thompson (“ Dietetics ”) divides foods into six groups, as follows : (1) Water ; (2) salts; (3) proteids (chiefly albuminous and allied gelatins); (4) starches; (5) sugar; (6) 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 each furnish, respectively, of energy, repair of tissue, and heat ; for there are no more complex chemical processes known than those of metabolism. Foods have three kinds of values: (1) nutrient, (2) heat-producing, (3) force-producing. Caloric 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, investigators said: “ A healthy man needs so many gm. proteid, so many gm. carbohydrates, so many gm. fat,” etc. It proved inconvenient to reckon with three magnitudes, and to bring them into correct relation with the requisites of the individual organ- ism. Nowadays we compute the values of food-stuffs 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 (“ fuel value ”) — i. e., 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 measurement of this heat energy of food is called a calory. This capacity for heat production of foods is determined from the amount of heat which 44 PHYSIOLOGY OF DIGESTION. is liberated when any particular food-substance is transformed from its original composition when it entered the body, — by oxidation, — into those chemical combinations in which it leaves the organism. The unit for measurement, or the calory, signifies the amount of heat which is necessary to raise one kilogram of water i° C. I gm. of albumin furnishes 4.1 calories. I “ carbohydrate furnishes 4.1 “ I “fat “ 9.3 1 “ alcohol “ 7 “ Instead of saying a man requires 100 gm. albumin, 100 gm. fat, and 400 gm. carbohydrates, one now expresses this in calories, thus : A man requires 100 gm. albumin X 4-L 410 calories. 100 gm. fats X 9-3. 93° 400 gm. carbohydrates X 4 1 * 1640 “ Total, 2980 “ For every kilogram of body-weight, an adult requires, when at rest, a food-supply of 30 to 34 calories: during light occupation, a food-supply of 34 to 40 calories; during medium occupation, a food-supply of 40 to 45 calories ; during hard work, a food-supply of 45 to 60 calories. In very obese persons the requirements for food are less than the quantities stated by one-quarter to one-third. If the above calculations of the requisite number of calories per kilogram weight of any person are correct, and the supply maintained accord- ingly, the individual will maintain his weight. If the supply of calories is greater, he will gain weight; if the supply is less, he will lose weight. In a condensed statement of facts like the present, it will be ex- pedient to pass over the physiology of hunger, appetite, and thirst, which will be considered in the clinical part of this work (bu- limia, anorexia, etc.), and proceed at once to the study of digestion. Ptyalin Digestion. — Digestion really begins in the mouth, where the food is chewed into small bits and mixed with the saliva, which mechanically facilitates the mastication and deglutition. Chemical transformation also begins here, for the diastasic ferment of saliva — ptyalin — transforms a small portion of the starchy foods into maltose and dextrose. Ptyalin can produce this transformation of starchy foods only in an alkaline medium; accordingly the action ceases in the stomach; DIGESTION OF STARCHES. 45 but not immediately, however, as the conversion of starches into sugar goes on until the degree of acidity reaches I : 1000. As the ptyalin ferment becomes inactive in this acidity, the question arises, whether its activity is permanently destroyed by an acidity of I : iooo, or only temporarily, and whether it can resume its invert- ing power when the acid is neutralized. Boas, who attempted a solution of this, came to the conclusion that subsequent alkalini- zation, or diminution of the acid, causes the ptyalin to act again, so that in later stages of digestion, when the acid production ceases, the conversion of starch into grape sugar by ptyalin may be resumed, but the ferment never becomes as active as before. The existence of appetite is to a degree dependent upon the proper functioning of the salivary glands. Digestion of Starches. — In order to understand the various stages of starch conversion, it is essential to study the digestion of starch by ptyalin in the laboratory. There are recognized four stages of starch conversion, each distinct from the other, until dextrose is reached. 1. ( a ) This is common starch, representing a glue-like, muci- laginous jelly, not a clear solution, giving a dark-blue color with iodin in iodid of potassium solution. The next stage shows the first action of ptyalin. ( b ) Amidulin or Amylodextrin. — This still gives a distinctly blue color, though not so deep as No. I ( a ), with Lugol’s solution ; but amylodextrin is a soluble starch, and represents a real solution. 2. (a) Ery thro dextrin. — Gradually, as the inversion progresses, the color produced by the iodin solution becomes violet-blue, violet, red violet, red, or mahogany brown ; this modification is called erythrodextrin. (h) Achroodextrin. — With continued action of the ptyalin, a sub- stance is reached which gives no color with iodin ; this is called achroodextrin. Amidulin is precipitated by tannic acid and alcohol, but erythrodextrin and achroodextrin are precipitated by alcohol and ether, not by tannic acid. These two dextrins do not reduce Fehling’s solution, and do not ferment with yeast. 3. Maltose. — Soluble in alcohol, insoluble in ether ; reduces Fehling’s solution, but not Barfoed’s reagent (a four per cent, solution of cupric acetate to which one per cent, acetic acid is added) ; does not ferment with yeast. 4. Dextrose. — Insoluble in alcohol and ether; reduces Fehling’s as well as Barfoed’s solution ; ferments readily with yeast. 4 46 PHYSIOLOGY OF DIGESTION. It is important to familiarize one’s self with these reactions, as it often becomes necessary to determine the degree of starch conver- sion in cases of hyperacidity or supersecretion. It was formerly thought that the starch was first converted to dextrin, and this in turn was converted to sugar. According to Professor W. H. Howell (“Amer. Textbook of Physiology”), the starch molecule, which is quite complex, consisting of some multiple of C 6 H 10 O 5 , — possibly (C 6 H 10 O 5 )2O, — 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 and 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 iodin, and is known as erythrodextrin, while the other gives no color reaction with iodin, and is termed achroodextrin. It is pretty certain, however, that there are several forms of achroodextrin, and, according to some observers also, erythrodextrin is really a mixtuie of dextrins with maltose in varying proportions. In accordance with the general outline of the process given above, Neumeister proposes the following schema, which is useful because it gives a clear representation of one theory, but which must not be con- sidered as satisfactorily demonstrated: Maltose. Starch — Solu- ble Starch. Amylodex- trin. / Ery thra- y Maltose. r Maltose. ll dextrin. I Achroo- | f Maltose. f dextrin. a J Achroo- o L dextrin. 1 ) ) Achroo- l dextrin. (Malto- dextrin.) ^ Maltose. ( Maltose. 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 formed 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 GASTRIC JUICE. 47 the addition of small quantities of Lugol’s solution to the filtered stomach contents no longer produce any changes in color. The occurrence of a purple (erythrodextrin) or a blue color (starch) shows that the starch transformation has been incomplete. This may be due either to a deficiency of ptyalin or to a rapidly increasing acidity or hyperacidity of the stomach. Ewald states 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 carcinoma of the tongue. From the above it is evident that there must be two stages of gastric digestion, (i) an amylolytic and (2) a proteolytic. Having satisfied ourselves as regards the fate of the starches, let us pro- ceed to study proteolytic digestion, or conversion of proteids, gelatins, fibrins, elastin, etc. Gastric Juice. — Hydrochloric Acid . — The secretion of the stomach is a complex fluid, clear, colorless, and of acid reaction; it has only one-half per cent, of solid ingredients. The amount secreted in twenty-four hours is about 1600 gm. Its chief con- stituent is hydrochloric acid, which it contains in the amount of 0.1 to 0.22 per cent, (one to two per thousand). This degree of acidity is not reached at once, but gradually; at the beginning and end of stomach digestion the percentage of HC1 is considerably less. Besides the HC 1 , gastric juice contains two unorganized ferments, pepsin and rennin (or chymosin). Hydrochloric acid acts in six different ways, all of which are of great significance for the normal progress of digestion. 1. HC 1 acts as an antizymotic or antiseptic, destroying patho- genic organisms and preventing abnormal fermentations. This antibacterial effect extends even into the duodenum. 2. HC 1 has the power to convert the proenzymes of the gastric glands (pepsinogen and rennin zymogen) into active ferments in a very short time (according to Langley, in one minute). 3. This gastric acid possesses a certain regulating influence on the progress of peristalsis. 4. HC 1 transforms, with the aid of pepsin, albuminous bodies into peptones, gelatin into gelatin peptone, elastin into elastin peptone. But in reality the pepsin is the main or chief agent in these trans- formations, as the HC1 can be effectively substituted by nitric, phosphoric, oxalic, sulphuric, lactic, and butyric acids. 48 PHYSIOLOGY OF DIGESTION. 5. By HC 1 cane sugar is changed to invert sugar (dextrose and levulose). This property is also ascribed to a number of bac- teria that can invert cane-sugar, although after a longer time. 6. HC 1 , finally, is instrumental in bringing into solution the soluble calcium and magnesium salts, introduced in the food. Concerning the origin and derivation of the hydrochloric acid, we unfortunately have nothing but speculation. No free acid oc- curring in the blood or lymph, it is rational to conclude that it is produced in the secreting (oxyntic) cells of the gland-ducts. It seems probable that the acid is derived from the neutral chlorids of the blood, which are in some way decomposed, the chlorin uniting with hydrogen to form HC 1 . The acid is secreted at the gastric mucosa, while 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 chlorids. Ac- cording to Maly, the HC 1 is the result of a reaction between the phosphates and chlorids of the blood, as expressed in the following two equations : NaH 2 P0 4 -f NaCl = Na 2 HP0 4 + HC1 or 3CaCl 2 -f- 2Na 2 HP0 4 = Ca 3 (POJ 2 + 4 NaCl + 2 HCI. What is known thus far of the specific action of living cells en- forces the impression here, that, as in other chemical processes not yet understood, vital phenomena are difficult to express in chemical formulas. The gastric secretion is dependent upon innervation through the vagi. When the vagi are cut through in dogs (the right one in such a manner as to leave the inferior laryngeal and the cardiac rami intact — i. e. y below the point at which these nerves are given off, so as to preserve the sensibility and motility of the larynx and the cardiac innervation), the secretion of gastric juice ceases (J. P. Pawlow, “ Die Arbeit der Verdauungsdrusen ” [original in Russian], 1898, p. 72). PEPSINOGEN AND PEPSIN. 49 CHAPTER V. PEPSINOGEN AND PEPSIN.— RENNIN ZYMOGEN AND RENNIN.— INTESTINAL DIGESTION.— DUODENAL INTUBATION. It should not be understood that all combinations of the gastric juice with albumins are at once peptones; like the starches, the proteids reach their end stage of gastric digestion by a series of distinct intermediate stages. These are (i) proteid, (2) acid albumin or syntonin, (3) propeptone or hemialbumose, and (4) peptone. 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 egg, serum, and plant albumins, gelatin, meat, fibrin, casein, etc. The steps in peptic digestion may be made more intelligible by the following schema, modified from that of Neumeister (“ Lehr- buch d. physiol. Chemie,” 1893, p. 187) : Proteid Syntonin Primary proteoses, Protoproteose Heteroproteose. Secondary proteoses, Deuteroproteose Deuteroproteose. Amphopeptones, Peptone Peptone. No other mineral acid gives so good results with pepsin as HC 1 , which can form pepsin from pepsinogen in the shortest time. It is useful to be able to test for propeptone formation. In normal digestion, one hour 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 most expedient method, up to present date, is by means of the biuret reaction. In this reaction a dilute solution of cupric PEPSINOGEN AND PEPSIN. 50 sulphate is added to stomach contents in the cold, and a few drops of potassium hydroxid added sufficient to make the solution alka- line ; an intense red color results. Cupric sulphate and KOH, added to ordinary albumin and syntonin, without warming, pro- duces a bluish violet, which must be distinguished from the purple- red of biuret. The more marked the propeptone reactions are, the less the pep- tone which has been formed and eventually removed from the stomach. We can approximately estimate the amount of the pep- tone by the intensity of the biuret reaction if we always use the same quantities of stomach contents, caustic potash, and cupric sul- phate, and compare it with the reaction given with a peptone solu- tion of known strength. One hour after an Ewald test-breakfast, given to a person with normal digestion, propeptone is either not found at all or only in traces ; but in abnormally weak or slow digestion, propeptone is still abundant at that period. Peptone gives the same pink, purple-red color with the biuret reaction as propeptone. In estimating the rate of proteolysis in the stomach, the biuret reaction will not permit us to distinguish between these two bodies ; the only differentiation possible is by precipitation of the propeptone in the following 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 pre- cipitate will be propeptone, which can be filtered off and weighed ; any red biuret reaction after this separation must be due to peptone. In order to determine, in a given specimen of stomach contents, whether the pepsin or HC1 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, 3,4. To No. 1, nothing further is added ; to No. 2, enough HC 1 to make a solution of 2 to 3 per thousand (this can be accomplished by adding one or two drops of officinal HC 1 , U. S. Pharm.,to 10 c.c. filtrate) ; to No. 3, 0.2 to 0.5 gm. (gr. iij to gr. vij) of pure pepsin is added, and to No. 4 both HC 1 and pepsin are supplied. A small disc of egg-albumen (which is prepared by cutting boiled egg-albumen into lamellae of uniform thickness with a micro- tome and punching out equal circles by a cork-borer) is added to each test-tube, and they are then put in the incubator at ioo° F. The rate at which the albumin is dissolved will tell us whether RENNIN. 51 the filtrate was perfect as regards the requisite amount of pepsin and HC1, whether pepsin alone, or HC1 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 can not be imitated in a test-tube, — i. e., the absorption of ready-formed peptones, — a seem- ingly delayed digestive process of egg-albumen discs in the test- tubes may in reality be due to a very active stomach filtrate. The amount of HC1 and the amount of pepsin must be in definite relation to each other. Excess of HCl is as much of a check as insufficiency of this acid. Rennin, chymosin, or pexin, the second gastric ferment, pro- duces a light, not very cohesive, coagulation of milk. This coagu- lation is a characteristic cake of casein floating in clear serum, more dense, not lumpy, more cohesive coagulation, than that produced by acids. This ferment is a constant constituent of the stomach contents, just as pepsin and pepsinogen. With a complete absence of the rennin and its proenzyme, one can with certainty conclude that the case is one of atrophy of the gastric mucosa. The demonstration of rennin ferment is carried out in the fol- lowing manner: Ten c.c. of raw, unboiled milk are placed in the incubator with 2.5 drops of stomach filtrate. If rennin is present, the characteristic milk coagulation will occur in a variable time (one minute to several hours, according to the quantity of fer- ment). * Occasionally, rennin, the perfect ferment, is not contained in the stomach contents, while at the same time rennin zymogen (pexin- ogen chymosinogen) is present. This is demonstrated, according to Hammarsten, by adding to the mixture just described 2 c.c. of a concentrated solution of calcium chlorid, CaCl 2 . If a rennin coagulum occurs, it follows that rennin zymogen is present, but not the perfect ferment. For these tests, raw milk only can be used, as it coagulates ten times as rapidly as boiled milk. Jaworski has pointed out that in cases where tests for rennin * The presence of peptone delays the clotting of milk by chymosin (E. Gley, “ Compt. Rend.,” 1896, 591. A. Edmunds, “ Journ. Physiol.,” xix, 474, 1896. F. S. Locke, “ Journ. Experim. Med.,” vol. II, p. 493). 52 INTESTINAL DIGESTION. and rennin zymogen are both negative, it is advisable to try pour- ing a 0.3 per cent, to 0.6 per cent, solution of hydrochloric acid into the stomach, to see whether this HC 1 may not be able to awaken a secretion of rennin ; this should especially be done before making the diagnosis of complete 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, con- tradictory. Concerning gastric digestion we are much better in- structed, 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, but hitherto all intestinal contents of human beings have been obtained from rare cases of intestinal fistulae, for the feces give no constant and reliable information of the digestive actions in the smaller intestine. The earliest investigations of intestinal contents were made in 1662 by Regnier de Graaf, who made experimental fistulae into the intestinal canal of animals. It is a curious historical fact that this intestinal experiment antedated 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 intu- bating the duodenum in the living human subject was devised by the author. This method, which is described in the “ Johns Hopkins Hospital Medical Bulletin” for April, 1895, and also in Boas’ “Archives for Digestive Diseases,” volume 11, page 85, consists, in the first place, of the introduction 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 ordinary stomach-tube, and has the exact shape of the human stomach when it is distended by blow- ing it up within that organ, to which it fits itself exactly, — and is closely applied to the gastric walls. The intragastric bag is distended by the pressure apparatus shown in figure 6. The graduated bottle ( A ) is full of water and elevated above the bottle (A), which is empty and also graduated. The stomach-shaped bag ( C ), when it reaches the stomach, is * The word “pexine” for this ferment, while etymologically and historically pre- ferable, has the serious disadvantage of sounding very much like the word “pepsin,” when rapidly spoken. The word “ chymosin ” avoids this possible confusion. PHYSIOLOGY OF INTESTINAL DIGESTION. 53 connected with the lower empty bottle, B. Then the stop-cock connecting A with 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 is observable on this bag, a guide is contained in it, running along the dotted line parallel 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. Fig. 5.— Apparatus for Obtaining Intestinal Contents. The relation of the thickness of the walls to the diameter of the lumen is shown in the cross-section of figure 5. When the intra- gastric bag is distended, it fills the stomach entirely. The duo- denal tube lies in its sheath or guide, and on being pushed onward from the mouth, it is not possible for it to go anywhere else except through the pylorus into the duodenum. In the illustrations it can be seen that the bag is not distended by the duodenal tube, but a separate, very small tube runs down the esophagus, ending in the bag, serving the purpose of its distention. Both tubes together do not occupy as much space as an ordinary stomach-tube. 54 DUODENAL INTUBATION. A description of this method is considered essential because it seems to be destined to bring our knowledge of the physiology and pathology of the intestines upon a basis of ascertained facts ; we can at any time thereby obtain the contents of the intestine, and 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 Fig. 6.— Pressure Bottles for Distending the Intragastric Bag during Duodenal Intubation. percussion sound on the outside of the abdomen, and the distance 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 electrodiaphany. Hitherto, in all experiments on this subject it has been impossible to obtain either the pancreatic or biliary secretion in a pure con- dition ; this is due to the fact that both the pancreatic and the common gall-duct empty into the descending portion of the duo- denum very near each other. THE PANCREAS. 55 In May, 1897, we had under observation a female patient who had suffered repeated attacks of biliary colic. At times she passed small stones without giving her much pain — at least they were found in the stools without having given her any colic. She was willing to undergo an operation to be relieved. Through the comparatively thin abdominal walls we were able to feel numer- ous stones in the gall-bladder. She consented to an attempt at intubation of the duodenum to determine whether there was any bile secreted. The duodenum was entered without difficulty, and cleansed by running in and aspirating out distilled warm water. Twelve hours afterward, no food having been taken in the mean while, the duodenum was again intubated accord- ing to our method, and washed with 100 c.c. of warm distilled water. On being aspirated, the water was still clear, but viscid and sticky, similar to a solution of egg-albumen. It contained no bile-pigments nor cholesterin, and was free from taurocholates and glycocholates. It was colorless and odorless, and seemed very rich in some form of albumin. That it was a solution of pancreatic juice was proved by its digesting fibrin and serum-albumin. The juice obtained in this manner digested from eighty-five to ninety-five per cent, of Merck’s dried serum-albumin in the diges- torium at ioo° F. in two hours. The amylolytic and fat-decompos- ing property of the juice was determined in a similar manner. One is therefore justified in concluding that in this case the pancreatic juice was obtained almost pure, as there were no bile elements con- tained in it, the bile being prevented from entering the duodenum by a calculus or catarrhal occlusion in the common duct. As there are also pancreatic calculi, or occlusions 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, from the human subject, without operation. The secretions of Brunner’s and Lieberkiihn’s 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 fundamental investigation concerning the pancreatic secretion. Later on Kuhne, Bidder and Schmidt, Corvisart, Heidenhain, and others amplified these results. Its secretion, as Bernard first observed, is dependent upon digestion, and is a clear, colorless, and odorless fluid, very alkaline, 56 THE PANCREAS. and so rich in albumin that it solidifies on boiling. Zawardsky had opportunity 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 per cent, water, 13.25 organic substances; among the latter are 9.2 proteid bodies and 0.83 extractive substances, soluble in alcohol ; lastly, 0.34 per cent, salts. The chyme which passes into the duodenum from the stomach comes under the influence of formed or organized and unformed or unorganized ferments. The formed or organized ferments are represented by bacteria, which bring about carbohydrate fermenta- tion, mostly in upper bowel, and proteid putrefaction, mostly in lower bowel. The unorganized ferments are contained in the pancreatic secre- tion, the bile, and in the succus entericus. The most important constituents of the pancreas are three ferments or enzymes: (1) an amylolytic, (2) a preteolytic, and (3) a fat-splitting ferment (adipolytic). According to W. G. Halliburton and T. G. Burton (“Journal of Physiology,” vol. xx, p. 106), pancreatic juice possesses a milk- precipitating substance, causing at 35 0 to 45 0 C. a granular precip- itate 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, and the milk resumes its granular fluidity. The granular precip- itate produced 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 quantities of dex- trin and grape sugar are formed ; one gm. of pancreatic juice from a dog will invert 3.6 gm. 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 glycerin.* This process occurs very * The form in which the fats are ultimately absorbed from the intestine is still a matter of hypothesis (Schafer’s “ Textbook of Physiology,” vol. I, article on Fat Absorption). The emulsion theory — i.e . , absorption as natural fat — and the solution theory — i.e . , absorp- tion as fatty acids and soaps — are both advocated by physiologists of prominence, so that no exact scientific conclusion in favor of either view is as yet possible. THE PANCREAS. 57 slowly, however. Berthelot found that fifteen grams of pancreatic secretion of the dog required at least twenty-four hours to break up two decigrams of monobutyrin completely into butyric acid and glycerin. The fatty acids formed during this transformation com- bine with alkalies in the intestine to form soaps, which, by emulsi- fying other fats, assist greatly in their absorption. In the laboratory it always requires 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 disease of the pancreas the feces become very rich in fat, which may be present in so large an amount as to congeal on the surface of the stool. The proteolytic ferment of the pancreas has been called trypsin by Kuhne. Digesting boiled blood-fibrin with pancreatic juice, he found that it did not swell up, but that it became very fragile, and finally liquefied. As we take in all of our albumin in a boiled or roasted state, which becomes peptone in the stomach and not solu- ble albumin, the question has arisen : Whence do we derive our soluble native albumin ? This is obtained from pancreatic trypsin digestion of boiled albuminous bodies, which changes them to albumin soluble in water, or at least in a weak saline solution, from which they can be precipitated by heat. The proteolytic action of trypsin takes place best in an alkaline or neutral medium, though it is still active in faintly acid media. Among the bodies formed from albumins and proteids under the influence of trypsin are a globulin that is insoluble in water, hemi- peptone and antipeptone, leucin, tyrosin, and asparaginic acid. Indol, which is found in the jejunum, is a product of bacterial action on albumins. A chromogenic body has been described by Tiedemann and Gmelin which has received the name tryptophan ; it is a result of advanced albumin decomposition. Trypsin, then, to sum up, changes proteids to peptones and soluble albumins, casein to casein peptones, gelatin to gelatoses and gelatin peptone, and elastin to elastoses and elastin peptones. In animals that have been deprived of their pancreas by oper- ation, only forty-four per cent, of proteid, fifty-seven per cent, to seventy per cent, of carbohydrates, and no fats at all, were absorbed, although four-fifths of the fats was split up into fatty acid and glycerin. 53 THE PANCREAS. The processes of tryptic digestion are briefly represented in the following schema, according to Neumeister: Proteid Deutero Albumose Amphopeptone Antipeptone Hemipeptone Leucin Tyrosin Aspartic acid Tryptophan Trypsin produces peptone from proteids more readily than does pepsin. On account of certain differences, chiefly recognizable in dialysis, between the end-products of peptic digestion or peptones and those of tryptic digestion, the name of tryptones is used by the author in reference to the latter. The principal secretory nerve of the pancreas is the vagus (Paw- low, /. c. } p. 73). The gastric chyme by virtue of its contained HC 1 stimulates the pancreatic secretion reflexly by acting on the duodenal mucosa. Starch is no exciter of pancreatic secretion, but it augments the amount of amylopsin contained in it. Fat is a marked stimulant to pancreatic secretion and augments its amount of steapsin. Solutions of alkaline and neutral salts inhibit the action of the pancreas. The physiological excitants of the gastric secretion are the extractives (bouillon), while acids, fats, and even water are the physiological stimulants to pancreatic secretion. CHAPTER 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 duodenal chyme is significant on account of its alkaline reaction and its effect on the mucous membrane. The most important function of the bile is the excretion of metabolic products that can not be utilized in the organism. The contents of the gall-bladder represent a concentrated secre- tion ; therefore our knowledge of the physiological action of the bile depends upon the discharge of biliary fistulae. 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. Albumins increase, fats diminish, this quantity, while sugar and carbohydrates appear to exert no influence (Voit). The quantity secreted in twenty-four hours averages from 500 to 600 c.c. (Ranke, Wittich, Hammarsten). According to Phaff and Balch (“ Journ. Experim. Med.,” vol. 11, p. 59), the daily quantity was 514.3 c.c., and the greatest quantity may be secreted at any time of the day, and stands in no definite relation to any meal. The quan- titative analyses of Hammarsten have given the following results : Solid materials, 1.62 to 3.52 Water, 96.47 “ 98.37 Mucin and coloring matter, o. 27 “ 0.91 Compounds of bile-acids and alkalies, 0.26 “ 1.82 Taurocholate, 0.052 “ 0.203 Glycocholate, 0.204 “ 1.61 Fatty acids, 0.024“ 0.136 Cholesterin, 0.048“ 0.16 Lecithin, .... 0.048 “ 0.065 Fat, 0.061 “ 0.095 Soluble salts, 0.676“ 0.887 Insoluble salts, 0.02 “ 0.049 At times a diastatic ferment is present in the bile ; it is not a specific constituent (Neumeister), but appears in the bile like the 6o BILE AND THE SUCCUS ENTERICUS. diastatic ferment which appears in the urine ; it seems to be identi- cal with the ptyalin zymogen of the pancreatic juice. When the bile is prevented from entering the intestine, albu- mins, gelatins, 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 resorbs 99 per cent, of fats, if not more than 150 to 200 grs. are given — i. e., only one per cent, appears in the feces, but on producing an experimental fistula conducting the bile outward, 60 per cent, of the fats are not util- ized (Voit). The subjoined 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 per cent, of tribenzoicin were decomposed by pancreatic juice ; with bile, the total amount. 3. By its alkalinity it accomplishes 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 (von Wisting, Heidenhain). 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, dissolved 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 Lieberkuhn, and was first studied in man by Demant after a herniotomy. This secretion has the color of light Rhine wine, and is very strongly alkaline, owing to the presence of 1.5 per cent, carbonate of sodium. The principal constituents are albumins and mucin. It contains also ptyalin and an inverting ferment, but has no effect on albumins and fats ; its purpose seems to be that of a neutralizer of the acids originating from fermenta- THE FORMED OR ORGANIZED FERMENTS. 6l tion of carbohydrates; its excess of mucin may be instrumental for the onward movement of the bowel contents. The Formed or Organized Ferments (Bacteria). — Proteids, carbohydrates, and fats are subject to decomposition in the intes- tines by bacteria. Fats are not decomposed to any considerable 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, which occur principally in the upper small intestine and leads to the formation of acetic, lactic, butyric, and carbonic acids, alcohols, and hydrogen. It is not known how much of the carbo- hydrates is decomposed in this manner. The putrefaction of proteids, caused by certain bacteria of the lower bowel, occurs chiefly in an alkaline medium. The first prod- ucts of this putrefaction are the identical bodies which are formed during pancreatic digestion — viz. : albumoses, peptone, amido-acids, and ammonia. But then the putrefaction goes still further; tyrosin is 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 ca- pronic, valerianic, and butyric acids. The gases formed are car- bonic acid gas, hydrogen, hydrogen sulphid, and methyl-mercaptan. As bacteria can produce peptone, it might be presumed that such product may be useful to the organism. This peptone is not made for philanthropic purposes — it is simply one intermediate, probably unavoidable stage in a long chain of decompositions. We can not measure the intensity of carbohydrate fermentation, but the aromatic end-products of proteid putrefaction can be approximately estimated by determination of the amounts of com- bined and ethereal sulphates occurring in the urine. The number of bacteria increases from the duodenum down- ward until they become enormously profuse in the colon. They also differ qualitatively. 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 5 62 BACTERIA NOT ESSENTIAL TO DIGESTION. we have returned to what seems a more logical belief, based on observations of Escherich, who held that bacteria contributed very little to the digestion of the infant, as they do not affect casein and fats, but only sugar of milk, turning it into lactic and carbonic acids and hydrogen.* Macfadyen, Nencki, and Sieber arrived at a similar conclusion in their now classical observations on adults (“ Archiv fur exp. Pathologie,” Bd. xxviii, 1891). One of their objects of study was a female with a fistula that opened the small intestine on the exter- nal abdominal wall, just at the end of the ileum. The entire colon was therefore excluded from the digestive act. As nearly all pro- teid putrefaction occurs in the colon, this case presented a chance to study the condition of absence of products of albuminous putre- faction and its effects. It was found 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 is detrimental, rather than advantageous ; inasmuch as the bacteria live at the expense of the ingested carbohydrates, 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 decad, is, accord- ing to our opinion, in its infancy. So, also, our knowledge of the pathogenic significance of intestinal bacteria. There is, undoubt- edly, 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 metabolism. For instance, Metschnikoff has demonstrated that the multiplication of the cholera vibrio is much advanced by the presence of torulae and sarcinae in the intestines. It is conceivable that bacteria wage war upon one another, as well as upon the cells of our tissue, and that we are benefited by this mutual self-destruction of our parasitic inhabitants. It is con- ceivable, also, that they fall a prey 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 observers to reduce the amount of indican * The work of Nuttal and Thierfelder shows that guinea-pigs can live on absolutely sterile food, the excrement of the animals being sterile also while they were under the control of the experimenters. HYDROCHLORIC ACID NOT ABSOLUTELY ANTISEPTIC. 63 and of the ethereal sulphates in the urine, which indicates a reduced putrefaction (see A. Lockhart Gillespie, “ Edinburgh Medical Journal/’ November, 1898, p. 428). The human stomach must not be regarded as an organ that can absolutely sterilize all food. The spores, being more resistant to HC 1 than the fully developed bacteria themselves, pass through the stomach uninjured. Miller assumes that at the height of digestion only, when the amount of HC 1 is greatest, the less resistant bacteria are killed. Bunge, some years ago, announced that the principal object of the HC 1 was one of sterilization. It is undeniable, from recent investigations, 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 (University of Berlin) demon- strated that the mouth contains large quantities of microbes ; in one unclean individual he estimated the numbers of mouth bacteria at 1,140,000,000. Of twenty-five different varieties occurring in the mouth, this observer was able to demonstrate twelve of the same in the feces. Nevertheless, the mouth bacteria, according to Lucksdorff, constitute only three per cent., while those entering through the food constitute ninety-seven per cent, of the bacteria of the intestine. There is no autochthonous vegetation of bacteria in the intestine ; they are all introduced from the mouth, or in the food, or reach thereby way of the circulation. (By autochthonous bacteria are meant such as are originally developed at the place 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 many kinds of bacteria are capable of producing these dis- eases 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 affec- tion, or at other times a very serious disturbance. This is the case with the bacterium coli communis, which is tolerated without detriment by the majority of mankind; but occasionally it is demonstrated as the producer of colitis, dysentery, and cholera nostras. The manifold forms of the catarrhal inflammations are explicable by the fact that the intestinal flora is also very manifold. These same bacteria are factors in the etiology of diseases of the perito- 6 4 INTESTINAL AUTO-INTOXICATION. neum, 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. Hans Hensen (“ Zeitschr. f. Biol.,” Bd. xxxv, p. 1 10) has shown that bacteria can penetrate natural and artificial membranes that allow diffusion. There are fine canals, passable for bacteria, that can not be demon- strated by the hemoglobin test. Great harm can be done to the general organism, and to special organs in particular, not only from this invasion, 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 individual’s own intestinal canal is spoken of as intestinal auto- intoxication. Not all auto-intoxications are of intestinal origin ; diabetes mellitus, for instance, is an auto-intoxication 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 intes- tinal 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-naphthol, bis- muth, creosote, bismuth salicylate — are themselves toxic, and in doses sufficiently large to reduce the number of bacteria to any considerable extent, are harmful to the body. The putrefaction of proteids, as measured by the relation between the amounts of the combined and ethereal sulphates in the urine, can only be tempor- arily 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 intestines 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 the selection of adapted, appropriate diet, by fresh air, moderate exercise, good sleep, pure water, and by the avoidance of overeating and overdrinking (Hemmeter, “ On Intestinal Putrefaction and Albuminuria/’ “ Maryland Medical Journal,” July 24 and 31, and August 7, 1897). EFFECTS OF THE ACTION OF SOME DIGESTIVE SECRETIONS. 65 CHAPTER VII. EFFECTS OF THE ACTION OF THE SEVERAL DIGESTIVE SECRETIONS.— METHODS FOR TESTING THE MOTOR FUNCTIONS OF THE STOMACH. When the gastric chyme enteis the duodenum, the albuminoid and proteid foods appear partly as syntonin, albumoses, and pep- tones, 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 traces of fatty acids. Water, according to the interesting investigations of von Mering, is absorbed only in very small quantities from the stomach. It ap- pears that fully ninety per cent, of all water taken into the stomach is passed into the duodenum; alcohol, and whatever is in solution in it, is absorbed readily. Grape-, milk-, and cane-sugar, also mal- tose, are absorbed in moderate amounts when they are in aqueous solution. When they are in alcoholic solution, larger amounts are absorbed. Dextrin and peptone 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 solu- tion. Simultaneously with this resorption, a more or less active secretion of water occurs into the stomach. This secretion in- creases or diminishes as the quantity of substances resorbed or taken up increases or diminishes. Secretion of water occurs even when no HC1 is demonstrable in the normal stomach. The chyme, then, as it enters the duodenum, 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 HC1. When the bile acts on this acid chyme, a resinous, flocculent pre- cipitate is deposited 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 granu- lar 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 HC1 by pancreatic juice, bile, and succus entericus. If any pre- 66 INTERACTION OF DUODENAL SECRETIONS. cipitation occurs as stated, pepsin is also thrown down and resorbed again or digested by trypsin. The bile does not disturb the pro- teolytic power of pancreatic juice (Claude Bernard). Boas and the author have shown that the clear duodenal chyme will digest 81 per cent, of serum-albumin in three hours ; at 40° C. its alkalinity was 0.8 per cent., Na 2 Co 3 . It was also shown that this duodenal chyme converted 25 per cent, of starch into maltose, and that it produced 12.1 per cent, fatty acids from neutral olive oil in three hours. Boas obtained his mixture of bile, pancreatic juice, and succus entericus from a patient who had most probably a duodenal stenosis and who vomited this chyme frequently. In the author’s experiments the duodenal secretions were obtained by his method of intubation of the duodenum. The contents of the duodenum are acid, even in cases where no HC 1 is secreted in the stomach. It was found in these experiments that the duodenal juices, when filtered, digested 85 per cent, to 95 per cent, of Merck’s dried serum- albumin in three hours at 40° C. The author’s results with starch conversion show that the filtered duodenal juices will digest 42 per cent, of starches, or rather convert them into maltose, which is con- siderably in excess of the figures obtained by Boas. The fat- splitting effect observed by us in this juice was nearer the result of Boas, for we found that 15.3 per cent, of fatty acids were obtained from neutral olive oil. In a case of biliary calculi, we 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 mucus mixed. The fat-splitting effect of pancreatic juice is improved by the presence of bile, as is also the amylolytic action of amylopsin. Demonstration . — The action of pancreatic juice obtained from a dog on neutral olive oil and on a solution of starch should be studied both with and without bile. Pancreatic juice plus bile will split up more fat and convert more starch into maltose than without bile (Martin and Williams). The effect of trypsin on pepsin is not definitely known, but it is probable that pepsin, being closely allied to proteids, is disintegrated by trypsin ; but in an acid solution pepsin checks the action of trypsin (Kuhne, Langley, Ewald, and Baginsky). According to Baginsky, rennin is destroyed by a neutral solution at room temperature. The ferment action of bacteria in the small intestine is limited to the carbohydrates. Discharges of food from fistulae of the small intestine show no fetid decomposition of albuminoids (Ewald and NATURE OF CONTENTS OF ILEUM AND COLON. 67 Nencki). The absence of proteid putrefaction in the small intestine is probably due to the rapid downward movement of the food mass in this portion of the bowel and to its acid condition. Carbohydrate fermentation yields mainly lactic acid, ethyl alcohol, carbon dioxid, and hydrogen. Macfadyen, Nencki, and Sieber found the chyme that passed over into the large intestine (the cecum) from the ileum to be 550 gm., with 4.9 per cent, solid residue in case the chyme was of a very thin consistence ; and 232 gm., with 1 1.23 per cent, solid residue, if the chyme was very con- densed. Both of these figures are the amounts passing in twenty- four hours. The shortest time in which food passed into the cecum after it was swallowed was two hours ; the longest period, five and a quarter hours. The reaction expressed in acetic acid was equal to one per thousand; the acidity is considered to be due to newly formed acetic acid, as the lactic acid and the HC 1 are neutralized by the succus entericus. This chyme contained one per cent, albumin ; also peptone, mucin, dextrin, sugar, lactic acid, sarcolactic acid, and traces of fatty acids ; it contained no leucin, tyrosin, urobilin, or ammonia. The characteristic products of albuminoid decomposi- tion were absent. Jaworski’s investigation on the contents of the large intestine, which were discharged from a fistula in the ascending colon, showed that the daily fecal discharge of 150 to 200 grs. was decidedly alkaline, and contained the products of proteid and albuminoid decompositions, viz. : urobilin, skatol, phenol, oxyacids, ammonia, leucin, cadaverin, ethyl and butyl alcohol, sulphuretted hydrogen, and methyl-mercaptan. In view of the fact that the putrefaction of albuminoids and pro- teids 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. Nencki found that when the food contained 70.74 gm. albumin, which represent 10.602 gm. nitrogen, the amount of solid material discharged from a colon fistula in twenty-four hours was 26.5 gm., with 1.61 gm. nitrogen, which represented 10.06 gm. albumin. From this it is evident that 14.25 per cent., or, in other terms, only one-seventh of the total albumin, is left for digestion in the colon, and that 85.75 P er cent, is re- sorbed from the stomach and small intestine. The intensity of putrefaction in the colon depends upon four factors : (1) The amount of decomposable albuminoid materials in- ULTIMATE FATE OF DIGESTIVE FERMENTS. 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 strong acid reaction, due to free acids, inhibits putrefaction. Bile assists in this inhibition. Hirschler has demonstrated that carbohydrates suppress putrefaction considerably ; this is due to the lactic, butyric, acetic, and carbonic acids caused by their fer- mentation. Albumin and peptone are absent from the contents of the rectum (feces), but are present in typhoid fever (von Jaksch). Peptone is found in all diseases that may produce pus in the evacua- tions — for instance, dysentery, tuberculous intestinal ulcers, per- foration, peritonitis, 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 dif- ficult one to solve, as our only method of detecting pepsin, chymosin, trypsin, and ptyalin is by their digestive activity. In all experi- ments of this kind the feces must be first sterilized by saturated solutions of thymol ; before using this it is well to exclude the action of peptonizing bacteria by filtering through a Pasteur filter. If we found in the glycerin extract of the sterilized feces a sub- stance which would dissolve boiled egg-albumen in a solution of 0.2 per cent. HC 1 , we should be justified in concluding that it was pepsin. If it did not digest in HC 1 , but in a one per cent, solution of sodium carbonate, it would probably be trypsin. For the demonstration of a diastatic ferment a dilute solution of starch is brought into the incubator with about five c.c. of filtered, sterilized feces. After a few hours the HC 1 and soda solutions of the boiled albumin are tested for peptone by the biuret reaction, and the diastatic test-tube is tested with a dilute solution of iodin in iodid of potassium. If the starch is unchanged, the solution will be changed to blue ; if not, the color will be brown or yellow. In this way we have confirmed the fact that pepsin is absent from the colon contents, but trypsin is at times present, since the perfectly sterile extract of feces will digest fibrin and albumin in alkaline solution. The digestive action of the succus entericus, which, according to Griitzner, has a weak fibrin-dissolving property, does not extend to the albumins, and therefore it will not confuse the result stated above as pertaining to pepsin and trypsin. FATE OF DIGESTIVE FERMENTS. 69 The chief digestive action of succus entericus is on the carbohy- drates. If peptone occurs in the stools, it is, in the author’s opinion, a product either of pepsin or trypsin digestion, not exclusively of bacterial origin. Undoubtedly, there are proteolytic bacteria — for instance, the bacillus subtilis of Ehrenberg, the proteus vulgaris of Hauser, the bacillus putrificus coli of Bienstock, and the bacillus liquefaciens ilei of Macfadyen, Nencki, and Sieber, all of which exist ordinarily in the human intestine; and their first products of action on albumins are the same as occur in normal pancreatic digestion, viz.: albumoses, peptones, amido-acids, and ammonia; but then the action continues uninterruptedly, ending in the forma- tion of decomposition products stated in a previous paragraph. The bacterial product of peptone is probably of no use to the organism in which it occurs — it is a first stage to proteid putrefac- tion, and these proteolytic parasites need peptone for their own existence. The remote possibility that only bacteria could produce peptone in the colon (feces) might be excluded by the fact that after sterili- zation of the feces by a saturated solution of thymol, peptone will, in some cases, still be produced when the above tests are made. It is due most probably to trypsin, which is present in the stools when 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 decide upon its source. Amylopsin and steapsin have not been demonstrated as such in normal feces. It is not known whether pepsin and rennin (chymo- sin) occur in normal feces. We have found a proteid-dissolving ferment in the stool, which acted in a one per cent, solution of carbonate of sodium only, and was studied, in a case of complete atrophy of the gastric mucosa, with total absence of HC1, pepsin, and chymosin, and also of 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 was observa- ble. The stools were not diarrheic. Escherich’s assertion that the colon bacteria do not live upon the food introduced, — as, accord- ing to his opinion, there is no digestible food left there under normal conditions, — but that they live upon the secretions of the walls of the colon, is certainly erroneous — if this statement of his view is 70 MOTOR FUNCTIONS OF THE STOMACH. correct (quoted from Mannaberg, in Nothnagel’s “ Erkrankungen des Darms,” p. 38). The conception of some writers on this subject that food mate- rials are completely used up in the digestive tube, is not proved by actual fact. Even meat, when eaten in a most digestible form, is found in visible traces undigested 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 part, 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 Testing the Motor Functions of the Stomach. — The motor or peristaltic function is the most important one. A man may be able to live without the secretory and resorptive functions of his stomach, as the intestinal digestion and secretion would suffice for amylolysis and proteolysis, and he depends upon the small intestine altogether for the digestion and absorption of fats ; so that even in the total absence of gastric resorption and the falling away of secretions of HC 1 , pepsin, and rennin ferments, life could be maintained. But if the motor function is interfered with, the food would remain 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 digested. When the limit of distention was reached, the food would be ejected as in pyloric stenosis and gastrectasia. In all cases of inhibition or loss of motor power, the secretory power is seriously disturbed, or may cease absolutely; so also the resorptive power. (See chapters on Supersecretion and Motor Insufficiency.) Many cases of total absence of gastric secretions have been reported in patients whose body-weight remained normal and their general health unimpaired. The stomach has been removed experimentally in dogs, and the animals continued to thrive without it, if precautions were taken to provide finely divided food.* * Schlatter, of Zurich (“ Med. Record,” 1897, Lll, 909), and Dr. Brigham (“ Journ. Amer. Med. Asso.,” Feb. 12, 1898) have successfully removed the entire stomach from human patients in whom the digestive process continued practically normal, at least up to the date of publication. Much is yet to be learnt from the future of these two cases. Even a year of artificial life under the constant care of physicians does not prove that the stomach can be dispensed with. TESTING THE GASTRIC MOTOR FUNCTIONS. J I There have been, up to very recently, six different methods pro- posed for determining the motor functions of the human stomach : the methods of Leube, Ewald and Sievers, Klemperer, Fleischer, Einhorn, and Hemmeter. Leube’s method of estimating the duration of gastric digestion — i. e. t to determine after a definite average time of six to seven hours after a meal of 50 gm. bread, 200 gm. beefsteak, and a glass of water, or two hours after an Ewald test-breakfast, whether solid contents are 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 Nencki, is not decomposed by acids in the stomach, but is converted, by the alkaline juices of the duodenum, into salicylic acid and phenol. He and Sievers found that the appearance of salicyluric 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 from forty to seventy-five minutes after taking one gm. of salol. Delay in its appearance will indicate a retardation in the passage of food into the intestines. Salicyluric acid is recognized in the urine by the violet color produced on the addition of neutral ferric chlorid solution. 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 occurred in the healthy individual varied from forty minutes to two hours. This was to be anticipated, as the period during which a test-meal may remain in the stomach may vary normally between two and three hours. A. Lockhart Gillespie found that in the dog salol was not decom- posed above the mid-ileum, and suggested that salol can pass un- changed through the stomach-wall and become altered in the blood* its derivatives appearing in the urine. The duodenum was severed close to the stomach, and the pyloric end of the stomach pulled through the abdominal wall. Although it was thus impossible for the drug to reach the bowel, the dog’s urine contained salicyluric acid, notwithstanding the complete failure of the test for that body in the contents of the stomach (“ Edinburgh Med. Journ.,” Nov., 1898). 72 METHODS FOR TESTING THE GASTRIC PERISTALSIS. CHAPTER VIII. METHODS FOR TESTING THE GASTRIC PERISTALSIS. — (Continued.) As Evvald’s salol test is not applicable in private practice, because of the frequent micturition that is necessary. It is impossible to examine females by this method for the same reason ; and, also, because the excretion of salicyluric acid depends upon the chang- ing 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 in twenty-four hours, after the administration of salol to healthy persons ; but in patients with impaired gastric peristalsis, the reaction continues to be distinct much longer — sometimes for forty-eight hours. According to Fleischer and Hecker, the duration of excretion of potassium iodid in the urine of healthy individuals varies from twenty-nine to fifty five hours ; of sodium salicylate, from twenty-one to twenty-nine hours ; and in cardiac and nephritic patients this may vary from eighty to ninety-six hours. It is evident that methods of so vari- able a character are not satisfactory for exact research; nor even, on account of the great loss of time, of much value for compara- tive tests. Klemperer’s method consists in the introduction of ioo gm. 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 two hours, all oil yet remaining is washed out by repeated lavage, dissolved in ether, and weighed after removal of the .ether by distillation. In the normal subject Klemperer could find but 20 to 30 gm. of oil; the remaining 70 to 80 gm. had passed into the intestine. If larger amounts are found, — for instance, 50 to 60 gm., or more, — they are, according to Klemperer, an evidence of motor insufficiency. This method requires much time and skilled chemical analysis, and is also open to the same objection as that of Leube. Fleischer (“ Spez. Path. u. Therap. d. Magen- u. Darmkrankh.,” p. 791) has proposed a method to determine the gastric peristalsis PLATE III. Author’s Method of Recording Gastric Peristalsis. Patient with intragastric bag within stomach and pneumograph in place, both connected with the kymograph. LIBRARY OF THE UNIVERSITY of ILLINOIS, PLATE IV. Author’s Method for Determining Location and Capacity of the Stomach. The apparatus, not including kymograph. G. Intragastric bag distended. F. The esophageal tube attached to it. H. Intragastric bag collapsed in the shape in which it is introduced. A. Graduated pressure bottle elevated, filled with water. B. Stop- cock. D. Lower graduated bottle, empty at first. The bag is distended after it is swallowed by connecting it at E with D ; the stop-cock. 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 amount of air in G is always known, and can be utilized as an indication of the gastric capacity. LIBRARY LiltNOlS.' IODOFORM TEST FOR GASTRIC MOTILITY. 73 by giving o.i gm. iodoform in a gelatin capsule during meals; this compound does not decompose in acid media, but does break down in the juices of the duodenum, which are less acid than those of the stomach, and one of its resultants is potassium iodid, which can be tested in saliva by starch paper, which, when dipped into the saliva, colors blue on being touched with a drop of fuming nitric acid. Naturally, the potassium iodid can also be detected in the urine; but the fact which gives this method the preference over Fwald’s salol test is that the KI can be detected in the saliva. This method gives varying results, as we have discovered. In twenty-three apparently normal cases in which we have tried it, the reaction coloring the starch paper first occurred just one hour after the meal in twelve cases ; in six cases it occurred first in one hour and twenty to twenty-two minutes ; in two cases, in one hour and forty-one minutes; and in one case, in two hours. In two cases it took two hours and a half to demonstrate KI in the mouth, after giving o.i gm. iodoform. 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 fifty-five to one hundred and five 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 and Sievers’, Klemperer’s, and Fleischer’s methods, it will be observed that the gastric motility was deter- mined 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 supposedly alkaline duodenum, and its subsequent appearance in the secretions and excretions (potassium iodid in the saliva and salicyluric acid in the urine) — an expression in terms of time being 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 here also the result depended upon the passage of something into the duo- denum. 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. 6 74 METHODS FOR TESTING THE GASTRIC PERISTALSIS. 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 possi- bility of solution of the problem. However, a second and most important 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 — (i) so that they may be made into a more homogeneous mass; (2) that they may be brought into thorough contact with the gastric juice; and (3) to stimulate the secretion of this juice by the mechanical stimulation of the walls of the organ. 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 fibers, which arise from the muscularis mucosae, and are spun around the bases of the gland tubules (see frontispiece lithograph of normal gastric mucosa) ; 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 has described, in the “ New York Medical Journal,” September 15, 1894, an instrument which records the gastric movements by dots on a narrow piece of paper. This apparatus consists of a ball about ^ of an inch (14 mm.) in diameter, which is made up of two hollow metallic hemispheres screwed together. Within this is contained a second smaller ball, which is attached to the outer sphere by a non-conductor so that it is insulated from it. The central smaller ball bristles with small metallic spikes which radiate in all directions from the center to the inside of the two 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 between the outer hemispheres and the spikes of the central ball — for two insulated wires, one connected with the hollow ball, the other 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 connecting the ball with another part of the apparatus, the “ ticker ” (very much like the instrument used at the stock exchanges for reporting the variations in stock by telegraph), each motion of it METHODS FOR TESTING THE GASTRIC PERISTALSIS. /5 will be recorded by lines or dots on the paper. The ball is swallowed and brought into the stomach by the aid of a draft of water. It must be borne 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 we experimented at the biological labo- ratory 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. Records were taken with the animal’s abdomen intact and com- pared with those taken 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 within the abdomen or exposed to view, provided in the latter case it is kept warm. In our experiments the animals were placed in a large metal case with a glass top ; underneath the animal holder about two inches of water was contained in the bottom of the case, which was kept at the desired temperature by a number of Bunsen burners beneath the case. Thermometers were suspended from different parts of the case to register 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 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 ; Engelmann carried on his pioneer work on the contraction of the involuntary muscle-fibers of the ureter. Phluger and Heidenhain have done similar accurate work on excised organs, and the results have been repeatedly confirmed by other competent investigators. These epoch-making experimentations are mentioned to em- phasize the fact that experiments conducted on organs isolated either entirely (Martin, Ludwig, Engelmann) or partially (Schatz, Phluger) are capable of giving perfectly physiological contractions or peristalses which differ nowise from the perfectly normal ones. It is frequently urged that these experiments, on account of the operations and the anesthesia necessary, do not present perfectly physiological conditions, and that therefore the deductions made therefrom are not logical, nor represent the true state of normal functioning. 7 6 METHODS FOR TESTING THE GASTRIC PERISTALSIS. It is undeniable that we never get at the absolutely exact normal functioning of an organ — the stomach, for instance — during an experiment, as ether and chloroform have an inhibiting effect on gastric peristalsis. But we are enabled to produce unconscious- ness of the animal after a brief ether narcosis by brain compression, after which the ether is no longer necessary, 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 us to the idea of using an intragastric thin rubber bag of the shape of the stomach to record the peristalsis, after many attempts with a small spherical bag that did not exactly fill out the entire lumen of the stomach, was the repeated observation that the small, round bag, such as Professor Moritz, of Munich, used, did not record every peristaltic movement that was visible to the eye when the abdomen was opened. We frequently noticed peristaltic constrictions of the antrum pyloricum when the rubber bag, of about 12 cm. 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 con- cluded, after three 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 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 dis- tended 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 so far as to fill it out completely. Our apparatuses has been demonstrated many times on a large variety of cases in the clinical amphitheater of the University of Maryland, and in the biological laboratory of the Johns Hopkins University, is adjusted with great ease. By a pneumograph the library UNIVERSITY of ILLINOIS. y6 METHODS FOR TESTING THE GASTRIC PERISTALSIS. It is undeniable that we never get at the absolutely exact normal functioning of an organ — the stomach, for instance — during an experiment, as ether and chloroform have an inhibiting effect on gastric peristalsis. But we are enabled to produce unconscious- ness of the animal after a brief ether narcosis by brain compression, after which the ether is no longer necessary, 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 us to the idea of using an intragastric thin rubber bag of the shape of the stomach to record the peristalsis, after many attempts with a small spherical bag that did not exactly fill out the entire lumen of the stomach, was the repeated observation that the small, round bag, such as Professor Moritz, of Munich, used, did not record every peristaltic movement that was visible to the eye when the abdomen was opened. We frequently noticed peristaltic constrictions of the antrum pyloricum when the rubber bag, of about 12 cm. 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 con- cluded, after three 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 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 dis- tended 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 so far as to fill it out completely. Our apparatuses has been demonstrated many times on a large variety of cases in the clinical amphitheater of the University of Maryland, and in the biological laboratory of the Johns Hopkins University, is adjusted with great ease. By a pneumograph the I author’s method for recording gastric peristalsis. 77 respiration is recorded separately, and thus one is enabled to differentiate the active from the passive movements. A separate seconds-pen gives on the same paper a record in time, so that the experimenter can tell at a glance the duration, beginning, and end of the peristalsis. While it is a most satisfac- tory apparatus for recording the motor function, it offers a reliable means of ascertaining the size and exact capacity, and finally the intragastric pressure. No apparatus hitherto devised combines these facilities in so simple a bit of mechanism ; for, taking away the kymograph, which should be in every medical school, its important parts are simply the intragastric bag and a mano- meter. In practice, a manometer connected with the intragastric bag will answer; with watch in hand the experimenter is able to count the peristaltic movements as they are conveyed to the column of water. 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 our first report ( loc . cit.) we stated that only such patients are taken as have become accustomed to the stomach- tube, as the nausea and vomiting first attending the initial intro- duction of the tube make an exact record impossible (we lay great stress here on the word exact). No intragastric instrument, not even Einhorn’s electrode, can be introduced the first time without some nausea. While this may not lead to emesis, it nevertheless has a great influence on the number of gastric movements, as most cases we have tried generally show more contractions in the first experiment than in any 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 instru- ment is used. Probably none of these apparatuses will 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, our intragastric bags are used regularly at the Uni- versity of Maryland Hospital, and exact results obtained thereby, even at the first attempt. Our objections to the Einhorn gastrograph are : (1) That no differentiation between the active and the passive movements produced by the diaphragm 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 ad- yS METHODS FOR TESTING THE GASTRIC PERISTALSIS. equately determined ; (4) that the slow but very extensive gen- eral tonic contractions — a narrowing down, as it were, of the entire stomach to one point in the center — 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 cm. 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, Einhorn’s apparatus marks an epoch in the history of the study of stomach motions and their physiology. It is the first attempt, and largely a successful one, to obtain their record by mechanical means. Passive motions caused by the pulsations of the aorta and the impulse of the heart ventricles against that part of the saccus caecus cardiae which touches the arch of the diaphragm, and also the respiratory passive motions due mostly to the muscles of res- piration, 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 a hysterical girl, who had no active stomach movements, no genuine peristalsis at all, all of her gastric movements being due to respir- ation and circulation. This girl showed a normal state of the secretions after an Ewald test-meal, but at the same time there was stagnation and retention of food. It is, therefore, most essential to be able to distinguish 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. It is necessary to distinguish between methods for physiological study of gastric peristalsis and methods for diagnostic or clinical- work. Our method is available mainly for the physiological and clinical laboratories, though it will give valuable information even without the kymograph. THEORIES CONCERNING THE MOVEMENTS OF THE INGESTA. 79 CHAPTER IX. HEMMETER’S METHOD FOR TESTING THE GASTRIC PERISTALSIS. Theories Concerning the Movements of the Ingesta. One of the intragastric stomach-shaped rubber bags which are used in our clinic consists of three separate compartments: the first filling out the pylorus, the second distending the middle por- tion of the stomach, the third occupying a small part of the fundus and the saccus caecus cardiae. (See “ N. Y. Med. Jour.,” June 22, 1895, p. 772, and the accompanying illustration.) Each one of these compartments records on the kymograph by a separate tambour. In the report referred to we made the assertion, from the results obtained with this bag, that in the human being most, if not all, of the peristaltic waves are executed by and start at the pyloric end. This statement was made before Moritz’s investigations were pub- lished in the “ Zeitschrift fur Biologie,” 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 and peritoneal surfaces. One week before our results were published in the “ New York Medical Journal,” Dr. S. J. Meltzer, of New York, published his results with direct and indirect faradization of the digestive canal, which demonstrated quite conclusively 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 resist- ance being found in the mucous membrane of the stomach. Percutaneous and direct faradization of the stomach, or intestines can not produce any contraction in these parts. Meltzer stated explicitly the kind of instruments used, — the sliding inductorium (Schlittenapparat) of DuBois Reymond, a Grove’s cell prepared anew for each experiment, — and also the distance, in every case, of the primary from the secondary coil. His device of including the sciatic nerve of an animal (nerve- muscle preparation of hind leg of frog, most likely) in the circuit is practical, and has for a long time been used in our laboratory. There is, however, a very important matter which physiologists 8o METHODS FOR TESTING THE GASTRIC PERISTALSIS. must insist on knowing, and which Meltzer does not state, per- haps because it was not very readily ascertained ; and that is, the number 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 Fig. 7.— Intragastric Tissue Rubber BXg, with three distinct parts and three separate outlets for recording the origin and direction of gastric peristalsis. Outside of the mouth the triple tube separates into 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 No. 1 records the contraction of the pylorus; part No. 2, the middle of the stomach; and part No. 3, of the cardiac end. (See double plate for tracings of this apparatus.) readily when the number of stimulations does not exceed 240 per minute. The best contractions are obtained at a much lower rate of stimulation. The vibrator on the DuBois Reymond inductorium was found, after months of experimentation, to send too many stimulations into the gastric muscle per second. Later on, when we used the THE MUCOSA A NON-CON DUCTOR. 8 1 Kronecker interrupter, in connection with a Jacquet chronograph, and no more than ioo stimulations per minute, it was found that the preantral 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 starve the animal for twelve hours, as for some reason yet unknown, the contractions are more unlikely to occur the sooner the experiment is made after the in- gestion of food. Still, it must be emphasized that the mucosa of the stomach is practically a non-conductor. We have had occa- sion to try this in the physiological laboratory, with a bit of healthy human stomach-mucosa which one of our students tore off from the wall of his stomach during experimental lavage ; the piece was fifteen mm. long, five to six mm. broad, and two to four mm. 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 apparatus (aspirator). This was followed by copious hematemesis, for which we were hastily summoned. In the stomach-tube, partly projecting from the lower opening, was a bit of fleshy substance, which, on micro- scopic examination, proved to be gastric mucosa. After the hemorrhage ceased, the young man was treated for one week as if he had gastric ulcer. 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 continuous circuit generated by a battery of three freshly prepared Grove’s cells, with a milliamperemeter, soon after it was found; the meter indicated but three milliamperes. As it was impossible to get this fresh piece of mucosa into the circuit perfectly dry, it is probable that the indication of three milliamperes was brought about through the conducting agency of the moisture on the outside of the tissue. In the biological laboratory of the Johns Hopkins University we have frequently had persons’ stomachs connected with the kymograph, and an intragastric rubber bag blown up to fill out their stomachs exactly. Through the intragastric bag ran two insulated wires, one ending in a small brass knob near the pylorus, the other coming out against the mucosa near the cardia in a similar knob. Every active and passive motion was recorded by a manometer pen (“ N. Y. Med. Jour.,” June 22, 1895, p. 77 1). But the strongest 82 METHODS FOR TESTING THE GASTRIC PERISTALSIS. faradic currents (distance of primary from secondary coil — o) could produce no contractions of the stomach. Dr. George P. Dreyer and myself held one of the poles in the right hand — the plus, for instance — while the negative was in the stomach ; with the left hand we touched the back of the person’s neck, thus completing the circuit. The current was so strong that it became intolerable to us. Although this current made its circuit through the patient’s stomach, it caused no contraction, as was evidenced by the manometer in connection with the intra- gastric bag. Frequently we could observe contractions of any skeletal muscle 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 mucosa may transmit a current, yet the muscular layer give no evidence of contractions. We do not wish to imply that it is absolutely impossible to contract the human stomach by electrical stimulation ; but the current required to effect this must be so strong that the experiment becomes hazardous. Einhorn (“Diseases of the Stomach,’’ pages 78-83) and Paul Cohnheim (“ Archiv f. Verdauungskrankheiten,’’ Bd. 1, S. 274) have described tiny bits of mucosa which are found in the wash- water and vomit of many gastric sufferers. We can confirm this observation, and add that we have found these pieces of gastric mucosa on washing out the stomachs of perfectly healthy persons. It has occurred to us that in 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 omitted that all stomachs experimented upon by our method in this series were washed out prior to the experiment to insure absence of current-interrupting food-particles in the organ. Moritz experimented with an apparatus very similar to ours, except that his rubber intragastric bag was round, not stomach- shaped. It did not, therefore, exactly and completely fill out the organ, nor did he use the graduated pressure bottles, by which it is possible to determine exactly how much air is blown into the bag. Instead of a pneumograph, he used a per- forated cork in one nostril of the patient, which was connected with a second manometer, writing on the Ludwig kymograph. PHYSIOLOGY OF GASTRIC MOVEMENTS. 83 The advantage of the pneumograph over this method must be ap- parent. The author’s first results appeared in print three months before those of Moritz in the “ Zeitschrift fur Biologie,” Bd. xxxii, which are perhaps the most important contributions to the physiology of the motor function since the investigations of Hofmeister and Schiitz (“ Archiv f. exper. Pathol, und Pharm.,” 1886, Bd. xx). In order that the mechanism of the gastric peristalsis may be better understood, it is well to bear in mind the arrangement of the mus- cular 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 part of the stomach near the pyloric end 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,” second edition, 1847, P a £ e I0 4 - (A pioneer piece of work, very fundamental and thorough in its observations, this book remains a monument to American physiological and clinical observation.) Recent observers describe this transverse band as the sphincter antri pylorici, and locate it at a distance of seven to ten cm. from the pylorus. In the antrum pylori 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 movements during digestion were first carefully studied on the human being by Beaumont ; his facts and errors have influenced physiologists more or less up to the present time. One can not fail to suspect that the stomach of Alexis St. Martin and its manner of peristalsis were too far from the normal to permit absolutely correct con- clusions. The extensive adhesions which Beaumont describes certainly acted at times as irritants, at others as impediments, to normal peristalsis. Professor W. H. Howell’s views on the gastric movements, as expressed in the “ American Text-book of Physiology,” page 317, will serve as an expression of a modern physiologist. He says ( loc . cit.) the movements occur in two phases : “ First, the feeble peristaltic movement running over the fundus, chiefly on the side of the great curvature, and resulting in pushing the fundic contents 84 METHODS FOR TESTING THE GASTRIC PERISTALSIS. into the antrum ; secondly, the sharp contraction of the sphincter antri pylorici, followed by a similar contraction of the entire mus- culature 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, 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 occurring at short intervals would result in putting the entire semiliquid 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 description given by Beaumont is substantially accurate. A portion of this description may be quoted as follows : ‘ The ordinary course and direction of the revo- lutions of food are, first, after passing the esophageal ring, from right to left, along the small arch ; thence, through the large curvature, from 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 one to three 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 described. The general result upon the food may be easily imagined. It be- comes thoroughly mixed with the gastric juice and any liquid which may have been swallowed, and is gradually disintegrated, dissolved, and more or less completely digested, so far as the pro- teid and albuminoid 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 semiliquid 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. CRITICISM OF THEORIES OF BEAUMONT AND BRINTON. 85 “The rhythmic spurting of the contents of the stomach into the duodenum has been noticed by a number of observers, through duodenal fistulae 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 differs from Beaumont’s, in assuming a central current of the food, moving from the pylorus to the cardia through the central long axis of the stomach. There are, according to this author, two cur- rents, one along each curvature running from the cardia to the pylorus, meeting and turning inward toward the center of the stomach in front of the pylorus, and then running back toward the esophagus as a single central current, there dividing to make again two currents as before, one along each curvature. According to Poensgen (“ Die motor. Verricht. des menschl. Magens,” Strassburg, S. 82), Reymond, Donders, and Lesshaft ap- proved of this theory; while Penzoldt and P"oster accept the great food-circle of Beaumont. Although we have made over fifty experiments on dogs, cats, and rabbits to observe a food-circulation within the stomach corre- sponding to these views, and although we have had an opportunity of seeing into the human stomach, through fistulae, during diges- tion, we have not been able to confirm, by actual observation, either Beaumont’s or Brinton’s views. While we have no new explana- tions to offer, it has occurred to us that the piston-like backward and forward movements of the food caused by the antral contrac- tions, and especially of the sphincter of the antrum, is a sufficient force to effect the mixture of the chyme with HC 1 and the fer- ments such as are found in it when it leaves through the pylorus. The movements do not differ essentially from those observed in the cat by Cannon (“Amer. Journ. Physiol.,” vol. 1). 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 movements 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 mixture is not proved to occur in every instance. In METHODS FOR TESTING THE GASTRIC PERISTALSIS. herbivora (horse, cow) the center of the food-mass in the stomach may be alkaline or neutral in animals killed one hour and a quarter after feeding. The almost vertical position of the stomach was unknown to Beaumont and Brinton. Like many clinicians of the day, they believed the organ was normally in a horizontal position, trans- versely across the upper part of the abdomen. The amount of force required to lift the food-mass in a vertical line upward is considerable ; it is necessary to imagine a still greater force to accomplish the vertical ascent on the side of the lesser curvature, in order to conceive of a simultaneous descent on the side of the great curvature, which descending current must inevitably interfere more or less with the ascending one. In a number of experiments in which the stomachs of animals on opening the abdomen were found in active motion, we inserted long needles through the gastric walls to determine the direction they would assume under the pressure of the ingesta. According to Beaumont, the ingesta moving from the saccus csecus along the greater curvature to the pylorus should compel the points of needles to be directed toward the pylorus when run through the greater curvature, and along the lesser curvature they should point toward 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 diges- tion, be directed toward the pyloric end. If needles are inserted to a distance of y 2 of an inch 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, while another points to the pylorus. Only when the needles are inserted very deep, so that they dip into the central or axial stream, can one 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 curvatures are strongly turned toward the cardia, but simul- taneously those few needles in the antral and pyloric portions 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 squeez- ing liquid and semiliquid portions into the duodenum, can be STUDIES OF PERISTALSIS BY X-RAYS. 87 obtained by the intragastric electric lamp when introduced during the height of gastric digestion. These lamps can be seen through the abdominal wall in dogs whose abdomens have been shaved, when introduced in a dark room, though naturally not quite so distinct as when the abdomen is opened. The author has studied gastric peristalsis in the human subject by means of the X-rays. (The original method was described in the “Boston Medical and Surgical Journal,” June 18, 1896, and con- sisted of introduction of a distensible rubber bag into the stomach. The X-rays were cut off by a coating of argentic oxid on the inner side of the bag.) A new application of the method of Boas and Levy-Dorn for locating the site of obstructions in the digestive canal by means of capsules filled with bismuth subnitrate — which cut off the X-rays, and are thus visible — was made by W. B. Cannon for the study of the gastric peristalsis in the cat (“ Amer. Jour. Physiol.,” vol. 1, p. 359, May, 1898). His results are valuable as confirming other recent experiments, indicating that the main peristaltic work is carried on by the pyloric end of the stomach. This was experi- mentally demonstrated by the author with the apparatus pictured on page 80 (“ New York Med. Jour.,” June 22, 1895). The fundus is not capable of exciting effective contractions. As will be shown further on, it empties the ingesta very gradually into the pyloric antrum ; it is more of a reservoir than a food titrator. The mixing, titration, and expulsion is carried on by the muscular antrum pylori. In the cat the stomach is emptied by the formation between the fundus and the antrum of a tube along which constrictions pass. The contents of the fundus are pressed into the tube, which, together with the antrum, is slowly cleared of food by waves of constriction (Cannon, loc. cit.). The author has made observations on human subjects with thin abdominal walls by the method of Boas and Levy-Dorn. Before the Rontgen ray apparatus the cap- sule of bismuth subnitrate could be seen oscillating backward and forward, sometimes slowly, sometimes with surprising rapidity, until it was pressed through the pyloric sphincter, which generally appeared to occur with a rush. But never was any circuit of the capsule observed, such as is described by Beaumont, Brinton, or adopted by W. H. Howell. With the method used by Cannon — i. e. y mixing subnitrate of bismuth with the food — it is impossible to judge of any movement of individual particles; only the general body and contour of the stomach as a whole become observable. 88 METHODS FOR TESTING THE GASTRIC PERISTALSIS. We agree with him that the food in the fundus is not moved to any considerable extent by peristalsis, but his further con- clusion that it is consequently not mixed with gastric juice, may be true of the cat, but does not apply to the human being. Food drawn out of the fundus by the Einhorn stomach-bucket, which can be seen before the X-ray apparatus, always contains gastric juice if any is secreted at all. In man the antrum does not form into a tube as in the cat, though an approach to this formation is made; during powerful contractions the impression is conveyed as though a second sphincter, about ten cm. above the pylorus, con- tracted and shut off the antrum pylori from the body of the stomach. The author has observed this axial food-current at the clinic in a female patient with very thin abdominal parietes, when the Einhorn intragastric lamp was introduced one hour after a meal. In animals with abdomen opened we have been able to see this lamp carried along the entire greater curvature, from the pylorus toward the cardia, during active digestion, but the occurrence 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 we have no evidence that it ever reaches that systematic circulation described first by Beaumont and Brinton. It should not be overlooked that if the observations of Beaumont of a complete food-circuit were really true and constituted the only movements in addition to the duodenal extrusion which the food- mass underwent, there must always be a mass of food in the center of the 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 theory of piston movements and central current 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 ( loc . cit.), Moritz ( loc . cit.), Goldschmidt (loc. cit.) and the author show, is very feeble indeed in its contractions, and hardly sufficient to propel food in any direc- tion ; yet, according to the above theory, powerful contractions are CONCLUSIONS CONCERNING PHYSIOLOGY OF PERISTALSIS. 89 ascribed to it; but as the preantral sphincter is only seven to ten cm. from the pylorus, it certainly can not be made accountable for the movements all around the cardia and the saccus caecus. The musculature of the fundic end has never been observed in peristaltic motion by us, excepting the peristalsis occasionally arising from the antrum and traveling upward over it. During active peristalsis it is in a condition of tonic contraction with the intragastric bag in the fundus ; we have estimated this to be equal to six to eight cm. of water (water manometer). Moritz, in his work on “ The Motor Function of the Stomach,” studiously avoids referringto 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 general tonus of the fundus to explain the saturation and softening of the ingesta by gastric juice. The contrasting relations of the fundus and antrum regarding active peristalsis are evident in the degree of pressure, as observed on a water manometer in connection with our triple intragastric bag. In the fundus the pressure is, on an average, equal to three to six cm. of water. The increase of intragastric pressure due to cardiac action is equal to one to two cm. (In this is included the pressure due to every new heart impulse and aortic impulse.) The inspiratory increase of pressure is equal to six to twelve cm. These are very nearly the figures Moritz obtained, and we add them here as merely in support, and confirmatory, of his views. Conclusions . — It is necessary to distinguish the movements ot the (1) fundus, (2) preantral portion, (3) antrum, and (4) pyloric sphincter. (1) The motor apparatus of the stomach is represented by its muscular fibers. Where these are most developed, the peristalsis is strongest ; where they are least developed, it is weakest. (2) The fundus has a thin muscular development, hence its peri- stalsis is insignificant, and consists in squeezing its contents into the tubular preantrum or prepyloric portion. (3) Waves of constriction along the preantrum press the food forward and backward through this portion until a mightier wave-impulse sweeps it into the muscular ampulla just in front of the pylorus, the antrum pylori. (4) The final expression into the duodenum is executed by the antrum, which may contract as a whole or form into two spherical muscular ventricles by a constriction (rarely). (5) A food circula- tion, in the sense of Beaumont and Brinton, does not occur. The physiology of the motor function has been dwelt upon 7 9 o ABSORPTION FROM THE STOMACH. more extensively than seems necessary in a condensed statement of gastric pathology, not only because it is the most important office of the stomach, but because we have become convinced that, in a large majority of disorders of secretion and absorption, an abnorm- ality in the motor function lies at the foundation. The exaggerated or diminished peristalsis can on careful exam- ination be detected sometimes before the secretory and absorptive anomalies are apparent. The secretory disturbances observed after section of both vagi are due, according to Contejean, to the motor paralysis caused at the same time (“Archiv. de Physiologic,” vol. iv, p. 640). A similar view is held by H. Borutteau (“ Phliiger’s Archiv,” Bd. lxv, p. 26). The relation between motility and secretion and absorption is not at all well understood. The peristaltic movements effecting a churn- ing motion are those mostly concerned in stimulating secretion ; when these movements are lost, secretion is generally disturbed. The last vestige of peristalsis 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 absorptive function is greatly reduced (atrophic gastritis, car- cinoma). In temporary arrests of these functions, the secretive and absorptive functions generally return with improved motility. In our drawing (frontispiece), the manner in which the deep ends of the fundus glands are encircled by fibers from the muscularis mucosae is very evident. From this it is conceivable that the func- tion of the gland-cells is in a manner dependent upon the contrac- tility of the fibers of the muscularis mucosae, which can not fail to influence the blood-supply to these cells (see Mall, on “ Circulation in the Dog’s Stomach,” chap. 1). CHAPTER X. ABSORPTION FROM THE STOMACH. Penzoldf s and Faber s, HerscheV s, Julius Miller' s, and Hemmeter s Tests for Gastric Resorption. Remarkable variations exist in the absorptive power of the gas- tric mucosa, not only in different animals, but in the same animals at different times and under varying conditions. Absorption is ABSORPTION OF STRYCHNIN. 9 1 largely influenced by gastric innervation and the quality, quan- tity, and pressure of blood-supply. Edkins in 1892 (“ Journ. of Physiol.,” p. 460) published experiments in which he introduced a measured quantity of salt solution into the stomach of cats after ligation of the pylorus and the cardia ; after an hour he recovered exactly the same quantity again. We have already referred to the work of von Mehring (“Therap. Monatshefte,” 1893), which, like that of Edkins, shows that water is not absorbed from the stomach. Peptone, grape-, milk- and cane-sugars, maltose, dextrin, and alco- hol are absorbed, and von Mehring demonstrated that a more or less active secretion of water from the walls into the stomach occurred simultaneously with the absorption, so that in his dogs with duo- denal fistulae he found a larger quantity of water came out through the fistula than the dogs had taken by the mouth. Bouley and Colin (Colin, “ Traite de physiologie comparee,” vol. 11, p. 91) intro- duced strychnin into the stomach of animals after ligation of the pylorus — or after it was paralyzed (as they claim) by vagotomy. It is stated by them that the effect of strychnin was rapidly evident in the cat, dog, and pig, that itwas retarded in the cow, and that there was no effect — at least, no serious effect — in the horse. Tappeiner (“ Ueber Resorption im Magen,” “ Zeitschr. f. Biol.,” 1880) intro- duced strychnin into the stomach of cats; 0.03 gm. of this alkaloid in an aqueous solution was sufficient to kill a cat weighing two kilos in eight minutes. Cats whose pylorus was tied succumbed to doses of 0.05 gm. and more only after an hour and thirty minutes or even later. When the strychnin solution contained alcohol, it was absorbed almost as rapidly as when the pylorus was not ligated. Similarly, chloral hydrate was not absorbed in aqueous solution, but readily in alcoholic solution, from the stomachs of dogs whose pylorus was ligated. In the experiments of Meltzer on the absorption of strychnin and hydrocyanic acid from the stomach of rabbits (“ Journ. Exper. Med.,” vol. 1, p. 529), it was found that six to ten milligrams of strych- nin introduced into the full stomach with the pylorus open would rapidly bring on tetanus, and it is intimated that absorption takes place in that case from the intestines, not from the stomach. When the pylorus is closed, even such large doses as 200 milligrams of strychnin, remaining for many hours within the empty stomach, with good circulation and with intact innervation of the vagi, do not produce any effect at all. The conclusion is justifiable that the gastric mucosa does not absorb strychnin to any considerable ex- 92 ABSORPTION FROM THE STOMACH. tent. From Meltzer’s experiments, which apply only to rabbits, it is not evident that the circulation of the stomach was good, for when the pylorus or the cardia is ligated, a normal gastric circula- tion becomes impossible. Injection of strychnin, stained with methylene-blue, into the submucosa (loc. cit.), which was in two minutes followed by tetanus, although the cardia was tied and a tube tied into the pylorus, does not prove that the circulation was normal. The same objections as can be brought against the experiments of Talma (loc. cit.) are applicable to Meltzer’s; the method constitutes too violent an interference with gastric circula- tion and peristalsis. The author has, however, been able to con- firm Meltzer’s conclusions, for in rabbitts in whom the pylorus was occluded by a rubber balloon introduced through the mouth and stomach and blown up in the duodenum just beyond the pylorus, it was discovered that strychnin is not absorbed from the stomach. Stenosing the outlet beyond the pylorus does not in any way injure the stomach nor disturb circulation or innervation. The rabbit is not free from objection as an experimental animal, as its gastric mucosa is rarely in an entirely normal condition. Meltzer found that distinct differences exist in the absorptive power of different parts of the digestive tract ; for instance, the mucous membrane of the esophagus absorbs strychnin very poorly. The part of the alimentary canal absorbing best is the pharynx ; the rectum absorbs strychnin next best, its resorptive power excelling that of the small intestine. Prussic acid is, however, absorbed very well from the stomach even when the pylorus is ligated ; it seems to produce a hemorrhagic surface on the mucous membrane which facilitates absorption. The method most commonly employed to test gastric resorption is that of Penzoldt and Faber. Three to five grains of iodid ot potassium are inclosed in a gelatin capsule, which is adminis- tered with ioo c.c. = ounces of water. Iodid of sodium or potassium, when taken internally, will appear, and can be tested for in the saliva and in the urine, where it is excreted in from six and one-half to fifteen minutes. The test is generally made by wetting starch paper with the saliva of the patient every two 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 iodid has reached the point of excre- tion, and consequently must have been absorbed. If this reaction first occurs after fifteen minutes, then the rate of absorption herschel’s test for absorption. 93 is reduced. This, according to Zweifel (“ Resorpt. Verhaltnisse d. menschl. Magens,” “ Deutsch. Arch. f. klin. Med.,” Leipsic, Bd. xxxix, p. 349, 1886), occurs in gastritis, dilatation, and carcinoma; in gastric ulcer the resorption is said to be normal, or nearly so. Most authorities (J. Wolff, Zweifel, Sticker, Quetsch) differ very much on this question, but agree on the reduced absorption in carcinoma. If the iodid is given during a meal, the reaction occurs much later. Herschel (“Indigestion,” London, 1895, p. 1 1 5) estimates the absorptive power by giving two decigrams of powdered rhubarb, which gives a red color in the urine with liquor potassae normally in fifteen minutes. Our experience with this method is that frequently the urine is so highly colored in digestive diseases 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 method. In the first place, Brandi’s experiments have shown that sodium iodid 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 soluble inorganic salts are practically not absorbed in the stomach, since it can not be supposed that they are normally swallowed in solutions so concentrated as three per cent. Brandi also found that condiments, such as mustard and pepper, and also alcohol, very much facilitated the absorption of sodium iodid. Perhaps, these substances act by stimulating the epithelial cells, or by causing a marked hyperemia of the mucosa. The absorption time does not vary much in the same individual, except when the stomach is full; in this case it is not only pro- longed, but is very variable in the same individual. This prolon- gation, according to Sidney Martin (“ Diseases of the Stomach,” London, 1895), is probably due to a considerable dilution of the iodid by the stomach contents, and also to the fact that the salivary glands are not so active 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 investi- gated, but also the excretory activity of the salivary glands. In Zweifel’s experiments it is probable, from what we know of the absorption of water in the stomach, through the observations of Tappeiner (“ Ueber Resorption im Magen,” “ Zeitschr. f. Biol.,” Miinchen, Bd. xvi, p. 497, 1881) and von Mehring {loc. cit.) y that 94 ABSORPTION FROM THE STOMACH. most of the liquid containing the iodid passes rapidly into the duo- denum. Therefore, we may be testing not only gastric absorption and excretory activity of the salivary glands, but also intestinal absorption. Zweifel concludes (loc. cit.) that in all diseases of the stomach there is a prolongation of absorption time, which is greatest in dila- tation and carcinoma and least in chronic gastric catarrh, and very slight in ulcer in the later stages; in the early stages of ulcer, how- ever, he claims, the rate of 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 estab- lishment of a diagnosis — is thwarted. In view of 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 and kidneys is a factor influencing absorption time, we have devised a method which is available for experiments on gastric absorption in the physiological laboratory, and which we have successfully tried on six male and eight female patients and ten healthy students. The methods of testing the urine and saliva were discarded entirely. Our method consists in washing out the stomach thoroughly; then, by means of our method of duodenal intubation, the entrance into the duodenum is plugged, or closed up, by introducing a small rubber balloon into it and blowing it up just in front of or beyond the pylorus. (A method having the same object in view has been described subsequent to the author’s publication, by Dr. F. Kuhn, in the “ Munchener medizin. Wochenschr.,” Nos. 27, 28, and 29, 1896, but it is founded upon a different principle from ours — the spiral sound.) After thus mechanically closing the pylorus, a weighed amount of any of the substances which von Mehring has shown are readily absorbed, or of any harmless inorganic salt, — sodium chlorid or sodium phosphate, — dissolved in 100 c.c. of distilled water, so as to make a three per cent, solution, is poured into the organ through a tube. This is indispensable to exclude loss of the salt solution through clinging to the tongue, mouth, and esophagus or absorption from these tissues. After a lapse of ten minutes the fluid is again drawn out of the author’s method for testing absorption. 95 stomach by aspiration, or even, if necessary, by adding known quantities of distilled water, until the last washing gives no indica- tion of containing any trace of the salt by a proper chemical test. 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 three per cent, solution is three gm. in case ioo c.c. are used — and the amount regained indicates the degree of gastric absorption. To simplify matters, the practical suggestion of Julius Miller (Boas’ “ Archiv fur Verdauungskrankheiten,” Bd. i,p. 237, “Zur Kennt. d. Sek. u. Resorpt. im menschl. Magen ”) has been utilized and can be recommended. It consists in noting the specific gravity of salt solutions before pouring them through the tube, and after any desired time, the solutions are washed out or aspirated, and the specific gravity again determined. The difference between these specific gravities taken before the salt solution enters the stomach and after it is regained affords a satisfactory index of the rate of absorption from the stomach if escape of the solution into the duodenum is prevented. It is not necessary to evaporate the whole solution to dryness in case sodium chlorid or any other harmless neutral salt is used. But after measuring the total quantity of liquid regained, — say, for instance, it amounts to one liter (1000 c.c.), — the amount of NaCl in ten c.c. can be determined by evaporation in platinum, and the weight of the total remaining NaCl calculated by multiplying the result by 100, or whatever the figure may happen to be. This method of determining the rate of gastric absorption gives approximately accurate results, even without duodenal intubation and mechanical closing of the pylorus, provided that by several preliminary experiments the motility of the patient’s stomach has been relatively determined. By observing what portion of 500 c.c. of water he will pass into the duodenum in, say, ten to twenty minutes, — this also requiring the drawing out again of the remnant of the 500 c.c. of water that was taken in for experiment, — von Mehring {loc. cit .) found that of 500 c.c. of water given to a large dog, through the mouth, the entire amount, or at least 495 c.c., had been passed out of the stomach through a duodenal fistula within twenty-five minutes. In the human being the passage of water out of the stomach is not nearly so rapid. Julius Miller {loc. cit.) found that the human stomach was not rid of even 200 c.c. NaCl. solution of the specific 9 6 ABSORPTION FROM THE STOMACH. gravity 1028 in thirty minutes. After this time he regained in one case 75 c.c. ; sometimes he regained more liquid than he poured in. In thirty tabulated measurements which he gives with sodium . chlorid solution (p. 240, loc. cit.), he regained more than he poured in, five times; the same amount, once; and a less quantity, twenty-five times. But his figures goto prove that even with an open passage into the duodenum, comparatively small amounts of salt solutions are passed out in fifteen minutes. Hence, if in any individual the average amount passing into the duodenum in fifteen minutes is known by previous experiments, the closing of the pylorus is not necessary to reach an approximate result concerning the rate of absorption. Miller confirms von Mehring’s conclusions that, contemporaneous with absorption, a secretion of water occurs into the stomach. This secretion increases with the concentration of the solutions. In the five instances mentioned where more was regained than was poured in, the specific gravities, which are a good indication of concentration, were 1066, 1061, 1052, 1088, and 1035. (Regarding the taste of three per cent, solution of NaCl, it might be explained that this is the percentage of salt in the water of the Atlantic Ocean, which has been recommended for internal use — A. Levertin, “ Hygieina,” xlvij, xlviii. “ Svenska lakaresallsk Forh.” S. 138, 1885.) In the studies with occlusion of the pylorus we experimented also with known solutions of sodium sulphate, peptone, maltose, cane-sugar, milk-sugar, and alcohol. As water is poured out on the surface of the mucosa, in return for salts absorbed, the specific gravity will not always instruct us as to the contents of NaCl, which had best be arrived at by weighing. From experiments on animals it is known that a concentrated solution may cause the stomach to secrete water, thereby diluting it, but that at the same time it is possible that there may be no resorption, so that weighing the residue from evaporating the liquid regained may be unavoidable for a correct result. Maltose was found a very practical substance for absorption ex- periments, though dextrose will also answer this purpose, as their quantity can be readily determined in solution by titration with Fehling’s solution, and also by the fermentation test, for which the Einhorn saccharimeter is most serviceable. Maltose will not reduce as much Fehling’s solution as dextrose, the exact relation TESTING ABSORPTION BY MALTOSE. 97 between the two being, according to Brown and Heron, for mal- tose, 60.8 ; for dextrose, ioo. According to Soxhlet, one c.c. Fehling’s solution corresponds to 7.78 milligrams maltose in one per cent, solution (provided the Fehling’s test was not diluted). Though maltose is converted into dextrose in the stomach, the amount converted in ten to fifteen minutes is, according to our observations, small enough to be dis- regarded. If desired, a test by Barfoed’s reagent may be made to detect if any dextrose is present in the liquid regained. The amount of sodium chlorid in the solution regained can also be determined by titration (Salkowsky u. Leube, “ Die Lehre vom Harn”; also, Neubauer u. Vogel, “ Analysen d. Urins ”). The method is given in the laboratory manual of Dr. Edward L. Whit- ney (“ An Introduction into the Laboratory Methods of Clinical Pathology,” p. 18, Baltimore, 1896). Our method for absorption testing is, in brief, the following: To determine the amount of 500 c.c. of a three per cent. NaCl solution passed into the duodenum in ten minutes: 1. Allow 500 c.c. three per cent. NaCl solution to run into a clean stomach through a tube and remain ten minutes. 2. Draw out as much as possible, washing out the last with known quantities of distilled water. 3. Determine the amount of NaCl as stated above, and add the average deficit of escape into the duodenum. The difference between the original amount NaCl and the amount regained is a fairly accurate index of gastric absorptive power; or, by our method of duodenal intubation, occlude the pylorus by blowing up a balloon in front of or beyond it ; pour into the stomach through a tube a known quantity — say, 100 c.c. — of a one per cent, solution of maltose; in ten to twenty minutes aspirate or wash out the amount of maltose left as above. The deficit will indicate the amount absorbed. 9 8 LOCATION, SIZE, AND CAPACITY OF THE STOMACH. CHAPTER XI. METHODS FOR DETERMINING THE LOCATION, SIZE, AND CAPACITY OF THE STOMACH. Percussion and Palpation. — Gastrodiaphany of Einhorn. Percussion of the stomach gives varying results, according to its contents and to the degree of its distention. The fundus is closely applied to the concavity of the diaphragm, and five-sixths of its volume is to the left of its median line; only one-sixth to the right (observe the accompanying illustrations from Eichhorst’s “Klin. Untersuchungs-Methoden ”). The highest point is the fundus, which reaches the level of the ninth thoracic vertebra. The lesser curvature runs along the left of the spinal column, and crosses to the right at the level of the first lumbar vertebra. The lesser curvature is entirely covered by the liver, and can be percussed or palpated only when it is located lower than normal. The pylorus is covered by the right lobe of the liver, about three to four cm. from the median line ; it is seven cm. lower than the cardia. The pars pylorica (antrum pylori) extends further to the right than the pylorus itself. The greater curvature in its upper part is largely covered by the lung ; its lower and anterior part is in appo- sition with the left hypochondrium and epigastrium. When the stomach is full, the greater curvature is two to four cm. above the umbilicus. To the right of the median line it ascends along the median edge of the gall-bladder, and is continued into the pyloric part. Distention very much facilitates percussion and palpation of the stomach. The conviction has been forced upon us that the degree to which the stomach can be distended is a very limited one. This state- ment is made after many hundred distentions with the intragastric stomach-shaped bag in connection with a manometer. Most stomachs that are in a normal state will refuse to be distended more than 100 c.c. beyond their natural capacity. Only in patho- logical thinning of the gastric walls and in atrophy of the muscu- laris is an overdistention conceivable ; even then some of the gases will escape by the cardia before painful distention will ensue. For these reasons distention with air or carbon dioxid is an DISTENTION OF STOMACH BY AIK OK C 0 2 . 99 expedient and safe way of determining the form and location of the stomach, and its relation to any tumors that may be present. There is no better way of differentiating gastric dilatation from gas- troptosis (falling) than by this process of distention. This method is carried out by introducing a stomach-tube, to the upper end of which is attached a double-bulb pump arrange- ment such as is used in some spray apparatus (Runeberg, “ Deutsch. Fig. 8.— Location of the Stomach — Dorsal View, i. Left kidney. 2. Right kidney. 3. Spleen. 4. Lungs. 5. Descending colon. 6. Ascending colon. 7. Complementary space occupied by expanding lungs in inspiration. 8. Hepatic flexure. 9. Splenic flexure of colon. The stomach occupies the space colored in red. Archiv f. klin. Med.,” Bd. xxxiv). Bouveret (“ Traite des Maladies* de TEstomac,” Paris, 1893) recommends that the air be forced into the stomach by blowing with the mouth through the tube. Riegel and Boas are very fond of gastric distention by carbon dioxid gas. A teaspoonful of bicarbonate of sodium, and about the same amount, or perhaps a little less, of tartaric acid, are dissolved, each in a separate glass containing 200 c.c. of water. IOO LOCATION, SIZE, AND CAPACITY OF THE STOMACH. First, the solution of tartaric acid is administered, and immedi- ately afterward the sodium bicarbonate. The patient must be in the dorsal position, with knees flexed. Within the stomach a brisk evolution of C0 2 occurs, at once distending the organ so that it stands out prominently, and is evident as a sharply defined, arched elevation. The greater curvature becomes very apparent; not so the lesser one. The patient should be told not to belch. The stomach under distention can be readily palpated or per- Fig. 9. — Location of the Stomach— Anterior View. 1. The stomach. 2. Liver. 3. Heart. 4. Lungs. 5. Complemental pleural spaces. 6. Trans- verse colon. cussed. If tumors were made out before, it is important to deter- mine their seat after the distention. It is possible thereby in many cases to demonstrate the connection or non-connection of the tumor with the stomach after distention. Accordingly, tumors which, when the stomach was empty, were palpated in the line of the umbilicus and to the right, for which reason it might be doubted whether they belonged to the stomach, after distention may move upward to the right, and toward the DISTENTION WITH AIR OR C 0 2 . IOI anterior arch of the short ribs. One may see and feel the direct transition of the tumor mass into the substance of the stomach, or trace its extent toward the pylorus, or ascertain that it is entirely independent of the stomach. Even the disappearance or the becoming less distinct of a tumor is very important, if it occurs after distention. This is observed in tumors of the posterior wall. If it is easily movable, very close i. Pronounced liver dullness. 2. Lesser liver ness. 3. Smaller heart dullness. 4. Larger heart dullness. 5. Limits of stomach percussion. 6. Traube’s semilunar space. 7. Left edge of short ribs. and tight adhesions may be excluded ; if it is absolutely immov- able, it is abnormally attached or fixed. It is evident that disten- tion of the stomach with air or gas not only enables one to get a better percussion area, but it serves another purpose: that of facilitating the palpation of tumors. Percussion and auscultation over the stomach frequently give valuable information concerning its boundaries without the 1 Fig. 10.— Normal Percussion Limit the Adult Stomach. — ( Eichhorst .) 02 LOCATION, SIZE, AND CAPACITY OF THE STOMACH. use of instruments. So does the elucidation of “ clapotement,” or splashing sounds. But when the stomach is not distended or no instrument is used, differentiation of colon from stomach becomes difficult, especially if the abdominal walls have any moderate thickness. Often mere inspection will disclose the loca- tion of the stomach when distended by its own gases. In his book on “ Diseases of the Stomach,” Riegel gives, in addi- tion to the above, ten other methods for determining location, size, and capacity, most of which, being more or less falla- cious, we must refer those specially interested in this matter to Riegel’s book, pages 41-56. In our opinion, all of these latter methods will, before many years, have only a historical value. There is one method for accomplishing the above objects, however, which we can recommend from a very large experience, and which is used extensively at our clinic, and of the accuracy of which we have had many opportunities to be convinced. With our stomach-shaped intragastric rubber bag (see plate iv) and the pressure bottles A and B, the location and capacity can be determined with great ease. The rubber bag used for this pur- pose has no sheath or guide for the duodenal tube. The stomach is distended by blowing up the bag within it; the amount of air necessary thereto is measured afterward by allowing it to escape into a spirometer. A less accurate, though quite practical method, is to catch the escaping air in a glass cylinder filled with water and inverted over a basin. It might be claimed that our method is a combination of von Kelling’s, Schreiber’s, and Jaworski’s methods, and it does indeed partake of part of the devices of all these. (See Riegel, pp. 51, 52, and 54.) Schreiber used a small, round, — not a stomach-shaped, — distensible balloon, but no pressure bottles nor spirometer. Jaworski used two pressure bottles, but no balloon or intragastric bag, and no spirometer, while von Kelling used simply the spir- ometer to measure the air, which he forced into the stomach with a double bulb, as is used on sprays. Our method of arriving at the capacity of the stomach is really, then, not entirely original, as it combines the best of the three older methods, but it is most convenient and reliable. The bag, as has been shown, can at the same time be used for determining the nature of the motor function. It can be asserted, from ’observa- tions on a large number of patients, that there is no other single method which is so useful, combining instruction concerning size, Fig. ii. — Stomach Distended by Air or CO*. Showing Stomach in State of Gastroptosis. — ( From the Author's Clinic .) 104 LOCATION, SIZE, AND CAPACITY OF THE STOMACH. location, and capacity of the stomach with that concerning its motor function. The method is as easy in its application as any which Riegel describes. The capacity can, for practical purposes, be read off on bottle B, from the amount of air that has been displaced into the intragastric bag. The cost of the bag is one dollar, and a good idea of the motor function can be had from a water man- ometer in connection with it after distention ; with one hand on the epigastric region, the respiratory movements can be felt, and thus distinguished from the active movements as expressed by the rise and fall of the water column in the manometer. It may thus be used without the kymograph.* Langerhans (“Archiv fur Verdau- ungskrankheiten,” Bd. in, S. 312) prefers the use of the intragas- tric rubber bag for the recognition of gastroptosis. GASTRODIAPHANY. Gastrodiaphany of Einhorn. — In 1889 Dr. Max Einhorn suc- ceeded in transilluminating the human stomach in the dark by means of a small Edison lamp attached to a soft-rubber tube ; from the lamp through this tube, insulated conducting wires ran to a storage battery. (See illustration, p. 105.) At some distance from the rubber tube was a current-interrupter. By this apparatus the inventor claimed to be able to ascertain the exact position and size of the stomach, and to recognize tumors and thickenings of the front wall by their lack of translucency. In 1867 Milliot had succeeded in transilluminating the stomachs of animals by platinum wires contained in glass tubes and con- nected with a Middeldorph’s apparatus. Fleischer, in his text-book (“Path. u. Therap. der Magen- u. Darmkrankh.” p. 789), claims to have succeeded, together with Hiifler, in transilluminating the human stomach before Einhorn. *In the shops of Baltimore small toy balloons are sold which are made of very thin but quite tough rubber, which my assistants have frequently used for intragastric disten- tion. These balloons accompany a game called “ pillow dex,”and are sold six for twenty- five cents. For studying the motor function they answer as well as the more expensive stomach-shaped bags, as I have assured myself that on distention they fill every inch of space in a dog’s stomach. P'or determining the capacity, however, the stomach-shaped bag is more accurate. ELECTR0D1APHANY OF THE STOMACH. 105 If this is really so, Fleischer did not publish his investigations, so far as we know, and certainly is not entitled to name the method after himself. To Einhorn is due the credit of developing the method as an aid to diagnosis. The patient, in a fasting condition, drinks from two glasses to a liter of water ; the apparatus is passed into the stomach just as the lavage tube is passed, and connected with the storage battery. The stomach transmits the electric light through the abdominal walls, becoming visible as a red zone at the place which corresponds to its location. The observation is executed in a dark room. In case the anterior gastric wall is occupied by a tumor, the light will not be transmitted at that spot, but all around it the rays will penetrate, thus evincing a dark, shaded area in a luminous zone. Fig. 12.— The Electrodiaphane. We are in the habit of marking the ribs, particularly the um- bilicus, xiphoid cartilage, and symphysis pubes, with phosphorus, so that they can be seen in the dark and serve as landmarks to the exact abdominal area in which the light permeates. In 1891 Dr. Howard A. Kelly prompted us to attempt transillumination of the colon by this method, and the author demonstrated it to the Clinical Society of Maryland in that year. Later Heryng and Reichmann (“Therap. Monatshefte,” 1892) published the first account of transillumination of the colon. The water-circulating diaphane devised by these clinicians, to prevent heating of the lamp, possesses no advantages whatsoever over Einhorn’s instrument. We have been able to illuminate, in successive portions, the entire colon in this manner, and demonstrated prolapse of the 106 LOCATION, SIZE, AND CAPACITY OF THE STOMACH. colon thereby. As the duodenum is but ten to twelve inches long, a diaphane of proportionate length has been introduced into the ileum in our clinic. We are not aware that this extension of electrodiaphany to the small intestine has been practised before we published an original device for intubating the duodenum ; it would be impossible without such a method. Notwithstanding the conservatism of Riegel and Fleiner (“ Lehr- buch d. Krankh. d. Verdauungsorgane,” p. 223) and the objections of Boas and Debove and Reinond, we consider the method valua- ble. It certainly is convenient for the rapid diagnosis and the differentiation between gastrectasia and gastroptosis. For the recognition of tumors, a much stronger light than that used by Einhorn — namely, eight to ten volts — may be useful, and one-half of the lamp coated by a reflecting mirror of mercury, which can, of course, be controlled by turning the tube outside of the mouth. At a demonstration which we were requested to give before the Clinical Society of Maryland (1891), the apex impulse of the heart was visible in the dark after transillumination. According to Einhorn, the method can be carried out both in the erect and the reclining position. He advises to permit the patient to drink only one to two glasses of water (200 to 450 c.c.), which amount will not distend the stomach beyond its natural capacity and position. When a stomach is distended with C 0 2 , or filled with water, it is unavoidably enlarged somewhat. Heryng and Reichmann recommend examining the patient in an erect posi- tion and with the stomach filled with from one to two liters of water. In this position and with that quantity of water, the organ can not fail to be increased beyond its natural size and moved out of its natural situation. Kuttner and Jacobson (“ Berliner klin. Wochenschr.,” 1893, Nos. 39 and 40) assert that the transillumi- nated area projected on the belly-wall does not correspond to the stomach alone, but also to light that is diffused through loops of intestine adjacent to the stomach, and filled only with gas. They found that the image is covered up wherever the liver is superim- posed upon the stomach, or intestinal loops filled with feces, or tumors of the anterior wall intervene between the source of the light and the abdominal parietes. It is possible to determine only the inferior and left lateral limits of the stomach by diaphany when the organ is in its normal position, for the lower edge of the liver prevents the transillumination of the remaining parts. It is therefore not possible to make the diagnosis of all cases of dilata- DISTINGUISHING DILATATION FROM PTOSIS. 10? tion by gastrodiaphany alone, for, as we shall show, there are dila- tations in which the stomach does not sink down to any marked degree. But in gastroptosis, where the stomach has sunk down as a whole and is adjacent to the anterior abdominal wall, gastro- diaphany will give characteristic pictures, and enable one to deter- mine both the upper and lower limits. When the stomach has sunk down, it loses its surface contact with the diaphragm, and therefore the transilluminated figure will show no respiratory movement. In dilatation the stomach lies in the normal position, or very nearly so, with its upper portions, which can not be transilluminated. In this condition the area of light on the belly-wall will show respira- tory movements on account of the contact of the stomach with the diaphragm. Kuttner and Jacobson hold that when the transillumi- nated zone shows distinct respiratory movement, the lesser curva- ture is in its normal position, and if the zone is below the umbilicus, — i. e low position of the greater curvature, — these signs together indicate a dilatation, provided transillumination through the intes- tines can be excluded. The so-called vertical position of the stomach may effect a low situation of the transillumination, but not a simultaneous respiratory movability of the lower light zone, because in this case the lesser curvature has moved away from the diaphragm. It is conceivable that gastrodiaphany may aid in the recognition of tumors of the anterior wall at a time when these can not be detected by other methods of investigation. In such cases the transillumination will be impossible because of thickening of the gastric walls. According to these observers gastrodiaphany is a valuable method for distinguishing between dilatation and gas- troptosis. Meltzing ( loc . cit.) made a large number of experiments on healthy individuals with the electrodiaphane, after which he came to the conclusion that the empty stomach occupies a larger area in the epigastrium than could be hitherto evidenced by percussion or gaseous distention. This is due, he argues, to the fact that per- cussion can only give the note from that portion of the stomach which is directly adjacent to the abdominal wall. The large curva- ture, however, is not adjacent, and therefore can not be made out by percussion. The same relative condition must evidently pre- vail when the stomach is filled with gas or water. This investiga- tor found that the greatest differences existed in the respiratory 108 LOCATION, SIZE, AND CAPACITY OF THE STOMACH. movability of the transilluminated area according to the position of the patient. He holds that it is not due to direct contact of the stomach with the diaphragm, and that movability which is evident in the reclining position may disappear almost entirely in the erect position. He declares that the differential diagnosis between dilatation and gastroptosis by the presence or absence of respira- tory movability of the illuminated area is not reliable. In a later publication Meltzing (“ Archiv f. Verdauungskrankheiten,” Bd. 11, . H. 4) attempted to prove the position of the electric lamp within the stomach by the use of a magnetic sound, and claims to have found that the results of both methods agree within the breadth of one finger. Kuttner, Jacobson, Renvers, Langerhans, Meinert, and recently Kelling have proved without doubt that the method is liable to give erroneous results. In the first place, the illuminated area may not belong to the stomach exclusively, and, secondly, we are not sure whether the location of the strongest intensity of the light really corresponds to the location of the lamp. These sources of error may arise in two ways : 1. The inferior border of the stomach may appear lower than the lamp really is — a deception which can be brought about when the greater curvature and the lamp lying in it are pushed away from the abdominal wall by a distended intestinal loop, and the irradiation is spread around this entire loop in a downward direction. When the lamp is allowed to wander along the greater curvature in a stomach filled with water, one may occasionally observe, during the transillumination, that a circular or elliptical very bright spot suddenly appears below the border-line of the gastric limit indicated by the passing lamp ; that this bright area does not belong to the stomach can be dem- onstrated by the high tympanitic tone which the circular bright spot will give on percussion. I have repeatedly observed this phenome- non during transillumination, and can not explain it in any other way than that the rays of light from the lamp are deviated ante- riorly through a distended intestinal loop superimposed partially on the greater curvature. I have also made several experiments on the dead subject in the method indicated by Kelling, — a number of the subjects were frozen before the experiment so that mova- bility of the abdominal viscera was impossible, — and been convinced that the transilluminated area was two inches lower than the real position of the lamp. 2. The lower border of the stomach may appear too high. This may occur when the lamp lying in the greater curvature is cut off CRITICISM AND LIMITATION OF THE METHOD. 1 09 from the abdominal wall by opaque objects not transmitting light — such as intestinal loops filled with feces or neoplasm. In order to obtain reliable results from gastrodiaphany, it is important that the patient’s bowels should be cleared out by enema, which will evacuate the colon, and about twelve hours before the enema is given a saline purge or a dose of castor oil will remove fecal accumulations from the small intestine. The bladder must be emptied before the examination, for when the stomach is very low, it has in some of my cases been superimposed upon the bladder, and the latter was found to be capable of being transilluminated by the light in the fallen stomach. This precaution is especially necessary when it is desired to illuminate the small intestine. We have experimented with incandescent lamps requiring a current of from eight to ten volts. This intensity of light, while it is of advantage when it is desirable to determine the topograph- ical limits of palpable tumors, is a disadvantage when we wish to simply transillumine the gastric wall that is free from neoplasm. The stronger the lamp is, the more deceptive will be the irradiation through adjacent loops of the intestine and colon. The most important literature of the subject is presented by Oppler, volume hi of the “Archiv fur Verdauungskrankheiten,” page 334. The following guiding maxims may be deducted from the literature, which I have subjected to a critical review to determine the actual value of the method ; these rules I know from personal experience are important to the practitioner in using this method : (1) The stomach of the patient must be empty and all remnants of food and gas must be evacuated as far as possible. (2) The intestine must also be evacuated of its contents and of gas by a purge and by enema. (3) The bladder must be evacuated. (4) The transillumination must be conducted in a completely dark room. (5) For determining the size and location of the stomach, a lamp of five candle-power should be used. For determining the limits of palpable tumors, a lamp of eight normal candle-power is advisable. (6) The diaphany should be conducted in the erect as well as in the reclining position. (7) In the reclining position the lamp gravitates away from the anterior gastric wall, and frequently no light effect is at all observable. Even in the erect position, when the empty stomach is transilluminated, no complete light image of the stomach can be observed on the abdominal wall, but only cer- tain undefined areas of light resembling spots or discs. (8) The results of diaphany correspond more and more closely to the real I IO LOCATION, SIZE, AND CAPACITY OF THE STOMACH. condition, the thinner and freer from fat the abdominal walls are. - In cases where the walls are thin, the limits agree well with the actual limits of the stomach, but, as a general thing, those obtained by diaphany are somewhat lower than the actual limit of the stomach. (9) If the lamp is allowed to glide along the greater curvature of the empty stomach by drawing out the tube, a series of light spots will be observed, which will indicate approximately the position of the greater curvature, provided a lamp has been used not exceeding four to five candle-powers, and only the bright center of the light discs are taken into consideration. (10) Excessive development of fat in the subcutaneous tissue and omentum and strongly developed abdominal walls render the results of the illumination fallacious. This also occurs when a stronger lamp has been intro- duced, because in that case the more illuminated center of the light discs can not be recognized, and the adjacent organs will also refract the light. (11) Megalogastria, which has been observed in individuals with thick abdominal walls, seems to be due to this deception. But even deducting any possible irradiation of light beyond the limits of the organ, it is certain that the greater curvature of the empty stomach is at a lower level than has hitherto been assumed. This is not invariably the case, however, and from our own critical observations, conducted on a sufficiently large material, we consider such extreme variations as Meltzing described (loc. cit.) as exceptional. (12), When the stomach is filled with from 500 to 1500 c.c. of water, a continuous picture is obtained in form of a luminous disc. (13) By this method the lower edges of the right and left lobes of the liver and the anterior margin of the spleen can be accurately determined. The former shuts off the light at the right superior boundary, and the spleen at the left superior boundary of the luminous area. (14) When the stomach is thus filled, the position of the greater curvature is somewhat lower than in the empty stomach, and it is from four to ten centimeters lower in the erect than in the reclining position. Meltzing and Martius assert that a line connecting the anterior superior spines of the ilium is exceeded in the majority of cases. If a lamp of only four candle-powers has been used, we should consider a stomach illuminated beyond this line as dilated or prolapsed beyond a doubt. Much depends in these cases upon the strength of the light and the amount of water introduced into the stomach. (15) Concerning the respiratory movements of the illuminated figure, I should say that in my experience it moves downward distinctly CRITICISM AND LIMITATION OF DIAPHANY. Ill during inspiration when the body is in the reclining position, but in the upright position the movements are very slight, and in case there is gastroptosis, there are no respiratory movements whatever. In the rare cases of extreme dislocation of the stomach, we could observe no respiratory movement even in the reclining position. (16) Filling the stomach with 1500 c.c. of water lowers the greater curvature somewhat. If only 300 or 400 c.c. are introduced, the lower margin of the stomach may even rise a little higher than the line it occupied when empty. Full distention with water enlarges the transilluminated area toward the right of the median line. The method of electrodiaphany has been extolled by a number of investigators, and severely criticized by others. In the existing chaotic condition of the various opinions, and as the facilities for obtaining the electric current in physicians’ offices in the cities are becoming greater with every day, insuring a more frequent and extensive application of this method, the author considers it his duty to sift the opinions presented, and subject them to critical analysis, along the guiding lines of a large experience. No matter how classical or well established the authority that presents an opinion, a writer with an analytical mind will see the utility and results of any method through the spectacles of his individual experience. From that standpoint I feel justified in emphasizing the fact that electrodiaphany will give rise to serious deceptions unless sup- plemented by other well-established methods, and that the diag- nosis should never be based upon transillumination alone. Electro- diaphany can be satisfactorily replaced by other methods of examination. With these limitations, we believe the method to be a valuable diagnostic aid, serviceable for the determination of the normal and abnormal topography of the abdominal organs. The abnormal shape and situation of the stomach, so-called loop form and vertical position, may be easily recognized in many cases. In very rare cases diaphany may suggest the presence of a tumor that is not demonstrable by any other method. It may be possible to detect tumors on the lower edge of the liver thereby, and possibly enlargement, tumor, and dislocation of the spleen. It does not present a useful means to determine dis- turbances of the peristaltic functions or gastric atony. When a small quantity of water is introduced into a healthy stomach, the lower curvature should rise somewhat higher. If this does not I 12 LITERATURE ON GASTRODIAPHANY. take place, we might suspect gastric atony. If the transilluminated figure does not alter its size on introducing a small and then a large amount of water, this would be suggestive of motor insufficiency. When the luminous area shows up very low upon the abdomen, great caution is required to differentiate between (i) physiological megalogastria, (2) dilatation, (3) gastroptosis. The respiratory movabilities which we have already described do not suffice to make a differential diagnosis, for in megalogastria (normal large stomach), as well as in dilatation, the respiratory movability is often very slight in the erect position, and in gastroptosis there may be slight respiratory movement in the reclining position. Only in total gastroptosis do we find the respiratory movement entirely absent. These evidences suffice to show that electrodiaphany is useful only in association with other methods of clinical diagnosis. LITERATURE ON GASTRODIAPHANY. 1. Boas, “Ueber die Bestimmung der Lage und Grenzen des Magens durch Sondenpalpation,” “ Centralbl. f. innere Medicin,” 1896, No. 6. 2. Boas, “ Diagnostik und Therapie der Magenkrankheiten,” 1895, Theil 11, p. 148. 3. Boas, “Ueber den heutigen Stand unserer Kenntnisse von Pathol, u. Therap. der Motilitatsstorungen des Magens,” “Therap. Monatsh.,” 1896, Heft 1, 11. 4. Briiggemann, “Ueber den Tiefstand des Magens bei Chlorose.” Inaug.- Diss., Bonn, 1895. 5. Einhorn, “New-Yorker medicin. Monatsschrift,” November, 1889. 6. Einhorn, “Berliner klinische Wochenschrift,” 1892, No. 51. 7. Epstein, “ Die Anwendung der Gastrodiaphanie beim Saugling,” “ Jahr- buch f. Kinderheilkunde,” N. F. xli, Heft hi, iv. 8. Hirschler, “Ueber Gastrodiaphanie”; referirt nach “Wien, klinische Wochenschr.,” 1894, No. 31. 9. Heryng und Reichmann, “ Ueber elektrische Magen- und Darmdurch- leuchtung,” “Therap. Monatsh.,” Marz, 1892. 10. Kelling, “ Archiv fur Verdauungskrankheiten,” Band 11, 1896. 11. Kelling, “ Physikalische Untersuchungen iiber die Druckverhaltnisse in der Bauchhohle, sowie iiber die Verlagerung und die Vitalcapacitat des Magens,” “ Volkmann’sche Vortrage,” N. F. cxliv. 12. Kelling, “ Ueber die Fehlerquellen der Magendurchleuchtung,” “ Archiv fur Verdauungskrankheiten,” Band ill, Heft 1. 13. Kuttner, “ Einige Bemerkungen zur elektrischen Durchleuchtung des Magens,” “ Berliner klinische Wochenschr.,” 1895, No. 37. 14. Kuttner, “ Zur Durchleuchtung des Magens,” ebenda, 1896, No. 38. LITERATURE ON GASTRODIAPHANY. I I 3 15. Kuttner und Dyer, “ Ueber Gastroptose,” “Berliner klinische Wochen- schr.,” 1897, No. 20. 16. Kuttner und Jacobson, “ Ueber die elektrische Durchleuchtung des Magens und deren diagnostische Verwertbarkeit,’’ “ Berliner klinische Woch- enschr.,” 1893, No. 39. 17. Langerhans, “ Magendurchleuchtung und Magenaufblahung,” “Wiener medicinische Blatter,” 1895, No. 45. 18. Leo, “Ueber Gastroptose und Chlorose,” “Deutsche med. Wochen- schr.,” 1896, No. 12. 19. Martius, “ Naturforscherversammlung,” Wien, 1894; referirt nach “Wiener med. Presse,” 1894, No. 40. 20. Martius, “Ueber die wissenschaftliche Verwertbarkeit der Magensdurch- leuchtung,” “ Centralbl. f. innere Medicin,” 1895, No. 49. 21. Meinert, “ Zur Fragevon der diagnostischen Verwertbarkeit der Magens- durchleuchtung,” “ Centralbl. f. innere Medicin,” 1895, No. 44. 22. Meinert, “ Ueber normale und pathologische Lage des menschlichen Magens und ihren Nachweis,” ebenda, 1896, Nos. 12, 13. 23. Meinert, “ Zur Aetiologie der Chlorose,” Bergmann, Wiesbaden, 1895. 24. Meinert, “ Ueber einen bei gewohnlicher Chlorose des Entwickelungs- alters anscheinend constanten pathologisch-anatomischen Befund, und liber die klinische Bedeutung Desselben,” “ Volkmann’sche Sammlung,” N. F., 1895, 1 1 5, 116. 25. Meltzing, “ Magendurchleuchtungen,” “ Zeitschrift f. klinische Medi- cin,” Band xxvii, Heft 11, ff. 26. Meltzing, “ Die Controle der Magendurchleuchtung mittels der Magnet- sonde,” “ Archiv f. Verdauungskrankheiten,” Band ii. Heft iv. 27. Meltzing, “ Gastroptose und Chlorose,” “ Wiener medicin. Presse,” 1895. Nos. 30-34. 28. Mikulicz, “ Wiener medicin. Presse,” 1881, No. 45 ff., und “ Wiener med. Wochenschr.,” 1883, Nos. 23, 24. 29. Milliot, “ Internationaler medicin. Congress zu Paris ” ; citirt nach “ Schmidt’s Jahrbuchern,” Band cxxxvi, S. 143. 30. Pariser, “ Berliner medicinische Gesellschaft,” 6. Juli, 1892. 31. Reichmann, “Ueber die elektrische Durchleuchtung des Magens fur diagnostische Zwecke,” “ Gazeta lekarska,” 1896, No. 32. 32. Renvers, “ Verein fur innere Medicin,” 4, iv, 1892. 33. Rosenheim, “Berliner klinische Wochenschr.,” 1896, No. 13. 34. Schwartz, “Ueber den diagnostischen Werth der elektrischen Durch- leuchtung menschlicher Korperhohlen,” “ Beitrage zur klinische Chirurgie,” Band xxiv, Heft ill. 35. Van der Weijde, “ De Doorschijnung van de Maag,” “ Nederl. Tijdschr. voor Geneeskunde,” 1895, Deel 11, No. 12. 14 STOMACH-TUBE AND TECHNICS OF ITS INTRODUCTION. CHAPTER XII. THE STOMACH-TUBE AND TECHNICS OF ITS INTRODUCTION. Examination of Stomach Contents. — Test-meals : Their Effect upon the Amount of Acid Secreted. — Literature. No other kind but a soft elastic stomach-tube should be used, and before introducing it for the first time in any patient, we should always carefully instruct him or her regarding the object and utility of the procedure and its harmlessness. Whenever we can do, so we give very timid patients an opportunity of observing with what ease more experienced patients introduce the tube on themselves. This has a most comforting effect. Weak and old persons should always be treated on the bed, several thick towels being placed on the patient’s chest and beneath the chin ; if the case is to be ex- amined in an erect position, linen gowns are drawn over the breast and lap, or an additional rubber sheet to protect the clothing. Dr. Fenton B. Turck, of Chicago, has devised a useful rubber pocket, which is suspended under the chin during lavage, and protects the garments of the patients from the mouth discharges. If the throat and fauces are very tender (often found in excessive smokers), it is advisable to precede the introduction of the tube by spraying the throat with a three per cent, solution of cocain hydrochlorate or the following anodyne spray : R . Three per cent, solution of cocain hydrochlorate in • benzoinol, 2 fluidounces One per cent, solution of menthol in liquid vaselin oil, . fz of a fluidounce. Use in atomizer for spraying the throat. Mix. Every patient should possess his or her own tube, especially in private practice. In hospital practice a special tube should in- variably be obtained for every carcinomatous, syphylitic, and tuberculous patient, and its use limited to that particular person. After the tube has been used it should be carefully washed, first with soap and warm water, rinsed out by a current of warm water and disinfected by placing it in a six per cent, solution of carbolic acid or a saturated solution of boric acid or thymol, in which the instrument should be kept coiled until it is used HOW TO INTRODUCE A STOMACH-TUBE. 15 again. Much has been written about the construction of the lower end of the tube. The author’s experience is that the Ewald tube as pictured on page 124 answers every purpose. The lower end of the tube should be open, as there can be no doubt that this facilitates the entrance of chyme into the tube when the con- tents are drawn, and also the entrance and exit of water during lavage. Two larger lateral openings at opposite sides of the tube and about two inches apart, are advantageous for the same object. The Ewald tube possesses also six to eight smaller openings, which may not favor the aspiration of thick chyme, yet are valua- ble for lavage, when it is desirable to produce a mechanical effect on the mucosa by having many fine streams fall upon it. They have the disadvantage of rendering the tube more difficult to clean. When there is reason to suppose a gastric or esophageal ulcer, neoplasm, or stenosis, I prefer a tube that is closed at the lower end, because this form is more likely to pass over these structural abnormalities without injuring them. If the patient is quiet and composed, it is safe to let him introduce the tube himself even at the first opportunity, the main points to impress upon him being three : (1) To swallow several times when the tube has reached the root of the tongue ; (2) to breathe deeply and regularly; (3) to push the tube with both hands as soon as it has turned downward into the esophagus. Introducing the finger into the mouth to depress the tongue is rarely necessary. Involuntary or intentional coughing must be suppressed by exercise of self-control, as it will inevitably prevent the point of the tube from entering the esophagus and turn it back into the mouth. The more passive and quiet a patient, the easier can the procedure be carried out. In addition to the execution of lavage the stomach-tube is useful for the following diagnostic purposes : (1) To draw the contents of the stomach for chemical and microscopical analysis ; (2) to estab- lish the permeability of the esophagus; (3) to determine the lower border of the stomach by palpating the tube through the abdom- inal walls. This method was originally proposed by Leube, but has been deserted even by him on account of its inaccuracy. In many cases it is not possible to palpate a tube through the abdom- inal walls, and even where palpable, it is not possible to differen- tiate a dilatation from a descent or ptosis. It is very important to use graduated wide^mouthed, transparent glass bottles of about one quart (one liter) capacity for lavage. At I 1 6 STOMACH-TUBE AND TECHNICS OF ITS INTRODUCTION. least two such bottles are needed — one to pour the water into the funnel, the other to catch the outflow. This outflow should always be measured, and efforts to regain the entire quantity that has entered the stomach must be made before an additional supply is poured in. Neglect of this precaution may produce dangerous overdistention of the organ. It is not necessary to lubricate the stomach-tube with any oil or vaselin — there is generally mucus enough in the esophagus to facilitate the passage. It is sufficient to moisten it with water. In the “ New York Medical Journal ” for December 28, 1895, volume lxii, No. 26, page 822, a new double-current stomach-tube has been described by the author, through which the inflow and outflow goes on uninterruptedly at Fig. 13— Hemmeter’s Double-current Stomach Lavage Tube. A. Hard rubber inflow. B. Soft rubber double tube. C. Hard rubber part of outflow. D. Stop- cock controlling inflow. E. Reservoir. F. Outflow openings. G. Soft outflow tube. /. In- flow opening. the same time. This tube is recommended only as a time-saver for the spe- cialist in practice; the simple tube will fulfil every requirement ; it is the safest instrument, even though in lavage of progressed gastrectasia it may require much more time. From 20 measurements of female patients, the author has found that the average distance from the incisor, teeth to the deepest portion of the stomach is 55 cm., and in 36 measurements of healthy males the same dis- tance was found to be 60 cm. In cadavers this distance is in both sexes shortened by postmortem rigor, according to the author’s experience, it having been found to be 52.5 cm. on the average for females in 12 different subjects. In 12 male cadavers, the average distance from the incisor teeth to the deepest part of the stomach was 54 cm. In ten cases of dilatation of the stomach, the average distance from the in- TECHNICS OF INTRODUCING STOMACH-TUBE. II 7 cisor teeth to the deepest portion of the stomach, as measured by as rigid a sound as could safely be introduced, was 69 cm. The author, on visiting Professor F. Penzoldt, in Erlangen, in July, 1895, was surprised to find this pioneer of digestive pathology still advocating the use of a guide in the shape of a flexible stick or whalebone, which, during introduction, is inserted into the gastric tube to facilitate its entering the esophagus after it curves over the base of the tongue. In his most recent contribution to the subject, Penzoldt (Joe. cit., 27) gives minute details as regards the method of application of the Leitungsstab or Man- drin within the tube, and says that it should be oiled to facilitate its removal when the tube has reached the middle of the esophagus. He also suggests catching the tip of the lavage tube between the index and middle fingers of the left hand, which are inserted into the patient’s mouth, and bending the tip down over the base of the tongue until it enters the esophagus. This is the method advocated by his teacher, Professor Leube (Joe. cit. t 2), and also by Rosenheim (36). In the writer’s experience the intratubal whalebone guide and the insertion of the fingers into the patient’s mouth are superfluous. The tube can always be introduced without a guide, and without touching the patient. The main object is that the point of the tube, when it has reached the wall of the pharynx, Fig. 14. — Illustrating the Principle of Siphonage. Fig. 15. — Bulb Used for the Aspiration of Test-meals with Patients having Very Relaxed Abdominal Walls. A. Stomach end. B. End going to collect- ing flask. 1 1 8 STOMACH-TUBE AND TECHNICS OF ITS INTRODUCTION. shall be deflected downward. This will occur without exception, and in a very natural, easy manner, if the patient is directed to swallow at this moment. In the moment of this act of deglutition the point of the tube is bent downward into the esophagus ; the physician must carefully watch this moment, and at the very onset of the act of swallowing rapidly push the tube over the descending epiglottis. If the patient should show difficulty in breathing after the tube is introduced, leave it quietly in place and encourage the patient to breathe deeply. Boardman Reed (“ International Medical Magazine,” Oct., 1898, p. 693) has correctly observed that the nervous spasm of the glottis occasionally encountered during the introduction is relieved by “ bringing into action the auxiliary respiratory muscles and making rhythmical forced inspirations.” Beginners in using the tube need have no fear that it will enter the trachea. To make it enter the trachea is, in the writer’s experience, a difficult undertak- ing, and requires special training and dexterity. He was present on an occa- sion when a class of ten students were taking a private course in diseases of the throat, during which lesson they were trying to mop the larynx. What they really did was to mop out the superior portion of the esophagus, showing plainly that it is not as easy to enter the larynx as the esophagus. Direct the patient to keep taking deep inspirations, and as soon as the tip or point of the tube is felt touching the pharyngeal wall, tell him to swallow, and almost immediately the tube follows into the esophagus and can be pushed into the stomach without further resistance. The double tube is still in its experimental stage and can not be recommended as practical. Personally, I use the single tube almost exclusively. It is not necessary for the patient to open his teeth any wider than just to admit the tube ; at the same time, caution him not to bite on it, but to breathe naturally. In case the tube is to be intro- duced into highly nervous and hysterical patients, or such who have not sufficient self-control, it is best to have their hands held by a trained nurse or assistant. It is always best to use both hands in pushing the tube. After it has passed the glottis, catch hold of the tube two inches from the mouth and rapidly complete the introduction. Avoid seizing the tube further away from the mouth, as then it will kink on pushing it. No patient should be subjected to gastric lavage without a previous examination of the thorax. Penzoldt tells of a case in which the stomach should have been washed out in the morning, but on account of lack of time this was postponed until the evening. On the same afternoon the patient died of rupture of an aortic aneurysm into the esophagus. Lavage and introduction of the tube are contraindicated — I. In all constitutional and local conditions which could be aggra- vated or life endangered by the irritation and exertion of lavage. Among these could be mentioned: 1. Pregnancy. CONTRAINDICATIONS TO LAVAGE. I 19 2. Heart disease in a state of defective compensation — heart neuroses, angina pectoris, myocarditis, and fatty heart in an ad- vanced stage. 3. Aneurysm of the large arteries. 4. Recent hemorrhages of all kinds, including apoplexies, pul- monary, renal, vesical, gastric, rectal hemorrhages, and hemorrhagic infarctions. 5. Advanced pulmonary tuberculosis. 6. Advanced pulmonary emphysema, with bronchitis. 7. Apoplexy and cerebral hyperemia. 8. Advanced cachexia. 9. Presence of continued or remittent fever. II. The stomach and intestinal diseases which are contraindica- tions for the use of tube are : 1. Ulcer, with recent hematemesis and evidences of blood in the stools. 2. Palpable carcinoma of the pylorus, with vomiting of coffee- ground material and the classical symptoms of cancer. 3. Stomach or intestinal troubles, with acute fever. 4. Gastric mucosa easily started to bleeding. 5. Secondary gastric affections whose dependence upon a distinct and more important primary disease is evident. These are not invariable rules, however ; cases may occur under some of these exceptions that at times peremptorily require lavage on account of depressing self-intoxication from the stomach or advanced gastric fermentation. Thus, according to Boas, it has been employed with success in pregnancy, and the author has washed out the stomach in cases of typhoid fever with favorable result, and also performed lavage in a case of aortic regurgitation, with Bright’s disease and gastrectasia, where much relief was experienced from the procedure. Professor Moritz has frequently passed the stomach-tube in pregnant women to ascertain the intra- gastric pressure (25). In a normal position of the abdominal viscera the location of the cardia corresponds to the spinous process of the ninth thoracic vertebra. By counting off this process on the back of the patient and placing the upper eye of the tube against it, one can measure the length of tube necessary to reach the stomach by applying it from this point along the back, passing alongside of the ear to the front incisor teeth. At this point, which reaches the incisors, it is of assistance to make a mark on the rubber with ink or to tie a 120 STOMACH-TUBE AND TECHNICS OF ITS INTRODUCTION. string around it; this will avoid passing the tube out or in to dis- cover whether it has reached the stomach after being introduced. In dilatations and falling of the organ, the length of tube required can only be learned after a previous lavage. When the tube is used to draw out a test-meal, direct the patient to contract his abdominal muscles as if in the act of having a stool. Frequently the accompanying nausea will bring this about involuntarily. If no contents arise, push the tube gently further in or pull it slowly out, trying different levels. If the abdominal walls are flabby, external manual compression will sometimes produce the desired result. If all these manipulations are of no avail, the stomach is either empty or the tube is plugged up with food-particles too large to pass. To find out which is the case, allow 300 c.c. of pure water to run in and then lower the funnel and siphon out ; if nothing but com- paratively clear water returns, the test-meal has passed into the duodenum. One should be very cautious in moving the tube out and in when no stomach contents appear in the funnel, as it is possible that the eyes of the tube may have sucked in the gastric mucosa itself, and by moving too suddenly, a piece may be torn away. If there is the least resistance, avoid moving ; rather force a little air through the tube with a rubber bulb or pour in a small amount of water, which will push away the adherent mucosa or the food-particle, and the next attempt will bring up the test-meal. If the stomach is already empty, the test-meal must be given again at another time. I do not recommend any apparatus for aspiration, not even the rubber bulb, except in cases of advanced dilatation or relaxed abdominal walls, when the rubber-bulb aspir- ator becomes necessary ; with patience the simple expression method will suffice. For small samples of test-meals the Einhorn stomach bucket (Einhorn, “ Diseases of the Stomach,” p. 63) is an available instrument. Before using the tube, all artificial teeth should be removed, and tight apparel, especially corsets, should be loosened. In very rare cases of intense food and mucous putrefaction, and in extensive gastrectasis, a recurrent tube may be used with success. To give an idea of the time it takes to cleanse some stomachs, we quote Dr. Herman Strauss, assistant to Professor Riegel, who claims to have washed out rice-particles after forty liters of water had been allowed to flow in and out. After person- ally washing a dilated stomach for one hour, we found bread and stringy mucus in the last washing. F. B. Turck asserts that food TEST- MEALS. I 2 I remnants, even after the stomach has been washed clear, may adhere to the walls of the organ ; for the removal of these he recommends his gyromele (“Chicago Clin. Review,” 1895). From examination of many hundred stomachs at autopsies we should judge that food adherence to the walls of the stomach occurs very rarely. Test-meals. — The test-meal most frequently employed is that of Ewald and Boas, consisting of a roll or a piece of wheat-bread and 500 c.c. of water or tea, without milk or sugar. The time for examination is one hour after the meal. Leube and Riegel advocate a test-dinner of 4CO c.c. soup, a por- tion of beefsteak or roast beef, potatoes, and a roll. The time for examination is three to four hours after this meal. Jaworski and Gluczinski employ the white of a hard-boiled egg and 100 c.c. water. Klemperer recommended y 2 of a liter of milk and 70 gm. of wheat-bread, and examined two hours later. WILLMP Fig. 16. — The Esophageal Tubal Probe. Germain See used 60 to 80 gm. scraped meat and 150 gm. white bread. Examination two hours later. The Ewald and Boas test-breakfast seems the most convenient, and in cases of enfeebled digestion, when much food is retained from previous meals, the least confusing. Fleiner’s test-meal consists of soup, roast beef, and potato puree; he examines three to four hours after the meal. Double Test-meal Used by the Author . — At our clinic, the Hospital of the University of Maryland, we generally use a double test-meal, consisting of : 8 A. m . — One small piece of beef, scraped and broiled =80 gm. ; 1 soft-boiled egg ; 30 gm. boiled rice ; 1 glass of milk = 250 c.c., and a piece of bread. Four to five hours later an Ewald test-meal is given, and one hour after this the stomach contents are drawn. In giving a test-meal, always insist on good chewing, and urge that all food substances be very finely cut up, so that they can not plug up the tube, even if not digested. 9 122 STOMACH-TUBE AND TECHNICS OF ITS INTRODUCTION. The double test-meal, about which the late Dr. Henry Salzer, of Baltimore, was quite enthusiastic, really offers some advantages over others. In the first place, it permits of as easy a study of the various stages of the digestion and of the motility and degree of retention as Riegel’s test-dinner; but the main advantage of the double test-meal — a full meal at 8 or 9 a. m. and an Ewald test- meal at 12 m. or 1 p. m., examination at 1 or 2 p. m. — is that, after drawing it, we may, in a large number of instances, recognize conditions of gastric motility and secretion before we analyze the contents. For instance, disappearance of the entire breakfast-meal points to a normal digestion. Absence of all proteids, — beef and egg, — and presence of consid- erable carbohydrates, — rice and bread, — points to hyperchlorhy- dria ; and, again, absence of all carbohydrates and presence of some of the beef and egg point to hypochlorhydria, subacidity, ana- cidity or achylia. Presence of the entire meal, with perhaps milk uncurdled, means impaired motility, with atrophy of gastric mucosa, absence of acid, enzymes, and proenzymes. If the entire meal has disappeared, the status of the gastric secretions may be ascer- tained from the Ewald test-meal, which is still present. The objection which has been made, that the double meal is uncleanly to handle during analysis, has also been urged against Riegel’s. Whether the morsels of an Ewald test-meal are nicer and more esthetic to handle than remnants of our double test-meal is a matter concerning which it does not pay to quarrel. It is a very important matter to state what test-meal is used in giving out the various acidities obtained, because some test-meals are greater stimulants to the gastric secretion than others. The Ewald test-breakfast really makes very slight demands upon the working capacity of the stomach. The total acidity one hour after an Ewald test-breakfast is nor- mally about 60*; the lowest total acidity observed by us one hour after a test-breakfast of this kind in a healthy individual was 22. Fleiner, who uses a test-meal of soup, roast beef, and potato puree, asserts that two to three and a half hours after this test-meal the total acidity is normally 70 to 100 (Prof. Wilhelm Fleiner, “ Lehrbuch d. Krankheiten d. Verdauungsorgane,” p. 186). Dr. Julius Friedenwald has confirmed that the gastric secretion of HC 1 *For the significance of these figures the reader is referred to the chapter on Titration of Stomach Contents. AMOUNTS OF ACIDS SECRETED AFTER VARIOUS MEALS. I 23 appears sooner, and reaches a higher degree after the double test- meal than after an Ewald meal. An amount of HC 1 equal to o. I to 0.25 per cent, may be regarded as normal; above this, is hyperacidity. The total acidity can not correctly be regarded as an unfailing indication of the amount of Fig. 17.— Stomach-pump used only for Rapid Evacuation of Poisons. HC 1 present; the latter should always be determined separately in addition to the total acidity. Apparently there are climatic, barometrical, and geographical fac- tors which influence the total acidity. In 170 cases at Riegel’s clinic, Strauss found the total acidity after a test-breakfast equal to 124 STOMACH-TUBE AND TECHNICS OF ITS INTRODUCTION. 68 ; in 92 cases at Berlin after a test-breakfast the average total acidity was estimated at 47 ; the average amount of free hydro- chloric acid at Riegel’s clinic was found to be 37. Normal values one hour after a test-breakfast of a roll and water are, for average total acidity, 40 to 60 ; for free HC1, 20 to 30, for our clinic at the University of Maryland, Baltimore, and in private practice. These were also the figures obtained formerly at the Maryland General Hospital. Four hours after the complex meal of Salzer, — i. e ., 50 to 60 grs. beef, 500 c.c. milk, 70 grs. rice, and one egg, — the total acidity on the average was found to be 95 and the free HC1 46, at the author’s clinic. It should be emphasized that these figures repre- sent only relative values. One often finds every symptom of hyper- acidity with relief following the use of alkalies, when the total acidity was found to be only 56 (one hour after an Ewald break- fast), the free HC 1 only 24. On the other hand, cases have pre- sented themselves showing, under the same conditions, a total acidity of 80 and free HC 1 = 50, still no symptoms of hyper- acidity. All this goes to show that some stomachs may do their work normally very well on relatively low amounts of free HC 1 , and, of course, suffer from hyperacidity from comparatively slight increase of free HC 1 , which would not affect a stomach used to higher amounts of acid. (See Hemmeter, “ Archiv fur Verdauungs- krankheiten,” Bd. iv, S. 30.) Most observers that can speak with authority on the subject agree that the total acidity should not be employed to express hyperacidity, but only the amount of free HC 1 , as this is the only acid which, when increased, gives rise to the complex of symptoms technically recognized as hyperacidity. Before closing this chapter it might be added that, where it is impossible to use the tube on account of prejudice of the patient, to obtain a test-meal, emesis may be resorted to. The stomach con- LITERATURE. 125 tents obtained after a test-meal, as a rule, filter slowly, and if much mucus is present, with great difficulty. The filtration can be accel- erated by rubbing the material first through a small, coarsely grained sieve (strainer), then through a finely grained strainer, and then filtered through Swedish filter-paper. LITERATURE ON THE HISTORY AND TECHNICS OF THE STOMACH-TUBE. 1. Abercrombie, “ Diseases of the Stomach." 2. Arnott, quoted by Alderson, on the “ Dangers Attending the Use of the Stomach-pump,” "Lancet," January 4, 1879. 3. Avicenna, “Liber Canonis," etc., 1544, Ausg. Venice, Liber 1, fen. iv, Chap, xx, p. 83. 4. Benedict, A. L., "Conservatism in the Use of the Stomach-tube,” "Am. Med. and Surg. Bull.,” 1898, xn. 5. Berger, C., " Ueber die Technik der Einfiihrung des Magenschlauches,” " Reich’s Med. Anz.,” Leipzig, 1898, xxm. 6. Bush, F., " London Medical and Physic. Journal,” 1822. 7. Canstatt, "Text-book,” Erlangen, 1846, Vol. in, Cap. vi. 8. Capivacceus, Hieronymus, " Medic. Practic.,” Liber 1, Cap. liii, Venice, 1590. 9. Dapper, " Die unbekannte neue Welt,” etc., Amsterdam, 1753, S. 566. 10. Ewald, C. A., " Klinik d. Verdauungskrankheiten,” Berlin, i890-’9i. 11. Ewald, C. A., "A Ready Method of Washing Out the Stomach,” " Irish Gazette,” August 15, 1874. 12. Hemmeter, John C., "An Apparatus'for Washing Out the Stomach and Sigmoid with a Continuous Current,” etc., "New York Med. Journal,” March 30, 1895. 13. “ Hieronym. Fabric, ab Abquapendente,” " Chirurg. Schrift,” ed. Joh. Scultetus, Niirnberg, 1716, 11 Theil, Cap. 39, S. 92. 14. Hieronymus Mercurialis, " Die Morbis venenosis et venenis,” Venetiis, 1583, Liber 1, Cap. 22. 15. Hunter, John, "Proposals for the Recovery of People Apparently Drowned,” “ Sammlung auserlesener Abhandlungen,” iv, S. 144. 16. Jackson, "Extracts,” " Records of the Boston Society for Medical Im- provement,” Vol. vi, p. 261. 17. Jlirgensen, " Zur lokal. Therapie der Magenkrankheiten,” " Deutsch. Archiv f. klinische Medizin,” Band vn, p. 239, 1870. 18. Knapp, M. J., "The Clinical Report of Four Cases of Lavage of the Stomach by the Aid of Knapp’s Director,” "Med. Rec.,” New York, 1898, liii, 313. 19. Kussmaul, " Behandl. d. Magenerweit. durch eine neue Methode, mit der Magenpumpe,” " Deutsch. Archiv f. klinische Med.,” vi, 455. 20. Leube, " Die Magensonde,” Erlangen, 1879. 21. Leube, "Deutsche Archiv f. klinische Med.,” Band xxxiii. 22. Martius and Liittke, " Die Magensaure,” Stuttgart, 1892. 126 LITERATURE. 23. Moritz, “ Zeitschrift f. Biologie,” xxxn, p. 314, Leipzig, 1895. 24. Murdoch, F. H., “The Use and Abuse of the Stomach-tube,” “ N. Y. Med. Jour.,” 16, 1, 1897. 25. Nicander, “Alex. Phar.,” Edit. Paris, 1857, p. 155. 26. “ Oribasius, Collecta medicinalia of,” Vol. viii, Cap. vi. 27. Pechlini, Joh. Nicol., “ Observation Physico-medical,” Liber 1, observ. 50, S. 1 16, Hamburg, 1691. 28. Penzoldt, F., “Allgem. Behandl. d. Magen- u. Darmkrankheiten,” in “ Handbuch der speciell. Therapie innerer Krankh.,” Vol. iv, p. 289. 29. Penzoldt, F., “ Die Magenerweiterung,” Erlangen, 1875. 30. Ploss, “ Der Magenkatheter a Double Courant,” etc., “ Deutsche Klinik,” 1870, No. 8. 31. Reed, B., “ How to Introduce a Tube into the Stomach with the Least Possible Embarrassment of the Patient,” “ Internat. Med. Mag.,” Phila., 1898, VII. 32. Rosenheim, “ Krankheit. d. Speiserohre u. d. Magens,” Wien und Leip- zig, 1891. 33. Rumsaeus, “ Organum Salutis, or an Instrument to Cleanse the Stomach,” l649 ' 34. Ryff, W. H., “Gross. Chirurgie,” Frankfurt-a.-M., 1559, Theil 1, p. 37. 35. Scultetus, Joh., “ Wundartzneyisches Zeughaus,” Frankfurt, Ulm, 1679, S. 108. 36. Socrates, J. C., “ Griindliche u. vollstandige Beschreib. d. Peniculi Ven- triculi Singularis,” etc., Lips. u. Frankfurt, 1713; “ Breslauer Sammlung von Natur u. Medizin,” etc.; “ Geschichten,” 1719, Classe v, Art. ill. 37. Sorbierus, in “ Sorberiana,” Paris, 1694. 38. Van Helmont, “ Doctrina inaudita de causa,” etc., “ Lithiasis,” 1646, Cap. vii, 34, S. 140. 39. Veronensis, Joh. Arculani, “ Practica,” etc., Venice, 1557, p. 82. 40. Welch, William H., Pepper’s “American System of Medicine,” Vol. 11, p. 607. ANALYSIS OF STOMACH CONTENTS. 2 7 CHAPTER XIII. METHODS FOR QUALITATIVE AND QUANTITATIVE ANALYSIS OF STOMACH CONTENTS. Presence of Bits of Gastric Mucosa. — Examination of Stomach Contents for Mucus, Saliva , Bile , Duodenal Secretions , Blood , and Pus. — Tests for Blood in Sto?nach Contents. — Demonstration of the Presence of Iron in Stomach Contents or Vomited Matter. — Spectroscopical Examination of Stomach Contents for Blood. — Examination of Portions of Mucosa or Tissue found in the Wash-water or Vomited Matter. — Literature. The stomach contents should be examined for — 1. The character and amount of the undigested food. 2. The presence and kind of bacteria and yeast fungi. 3. The bile, mucus, pus, and blood. 4. The total acidity. 5. The amount of free hydrochloric acid. 6. The presence of inorganic acids, as lactic, butyric, or acetic acids. 7. The combined hydrochloric acid and acid salts. 8. The presence of products of digestion, — viz., syntonin, pro- peptone, albumoses, peptone. 9. The presence of pepsin and rennin ; if these are absent, their proenzymes. 10. The products of starch digestion, dextrin, erythrodextrin, achroodextrin, and maltose. 11. Fragments of mucosa. 12. Fragments of neoplasms. Character and Amount of Undigested Food. — The exami- nation for undigested food-particles may demonstrate the presence of substances eaten twenty-four hours before the expression of contents, and thus, at once, establish an atony, dilatation, or stenosis. As already pointed out, excess of rice and bread and absence of beef and egg indicate a higher acidity, while absence of bread and rice and presence of egg and beef indicate sub- or anacidity. This, of course, can be most conveniently studied when the contents are drawn out about five hours after the first of the double meal, as employed by the author. 128 ANALYSIS OF STOMACH CONTENTS. Bacteria. — For bacteriological examination, a few slides are stained with methylene-blue, and also cultures made, the latter especially when there is any disease of the air-passages the microbes of which may get into the stomach with swallowed mucus or run down unconsciously during sleep. This is particularly important in pulmonary or laryngeal tuberculosis. Instead of methylene-blue, Lugol’s solution of iodin should be used on other slides for examining bits of tissue, mucosa, and cellular detritus. The normal stomach contains many micro-organisms ; only the presence of very large numbers of bacteria has a pathological significance, if by culture experiments they can be shown to be still capable of multiplication. Microbes only propagate luxuriantly when stagnation of gastric contents occurs. The secretory disturbances are then a secondary effect, a consequence of the stagnation. But primary reduction of HC 1 secretion has been known to cause a luxuriant gastric flora, since it is the HCl which, to a great extent, inhibits their develop- ment and also destroys a large number of them. If there be deficient peristaltic power, the diminution of HCl causes further disturbances in the stomach and intestines by accumulation of bac- teria. But no degree of gastric acidity, no matter how great, can destroy all bacteria introduced. Germ growth in the walls of the stomach and in adherent food- masses has been reported by F. B. Turck (“ N. Y. Med. Journ.,” Nov. 23, 1895). This has been observed by us in ulcer, ulcus car- cinomatosum, and carcinoma. Hyperacidity is as detrimental in its consequences as anacidity, because it inhibits normal intestinal digestion, which is the best means of combating fermentation and putrefaction. Hydrochloric acid undoubtedly inhibits or checks gastric fermentation to a cer- tain extent, but all ferment-producing microbes are not destroyed by it in the stomach. Therefore, one frequently finds gastric fermentation with hyperacidity of HCl, and, reversely, fermenta- tion may be absent where hydrochloric acid is entirely absent, provided the peristole is good. This will again impress the importance of an intact gastric peris- talsis, a certain time of action being indispensable for organized ferments to set up their characteristic decomposition even at the body temperature; with a good motility, however, the gastric chyme may reach the intestine, meeting a vigorous digestion BACTERIA OF THE STOMACH. 1 2g before the bacteria get a chance to forge ahead of the normal unor- ganized ferments. The most frequent of fungi in gastric contents is ordinary yeast, and there should be no difficulty in recognizing it. Unless occur- ring in large numbers and sprouting, it has no pathological signifi- cance. Two more germs found in the contents are of interest — the sarcinae and the Oppler-Boas bacillus, the latter occurring in the gastric contents of carcinoma. Sarcinae may be seen under the microscope without staining ; they are, indeed, preferably to be examined that way, as they stain so deeply with anilin dyes as to look like black patches. Sidney Martin recommends drying and fixing a drop of stomach contents on the slide or cover- glass, and placing in a very dilute solution of gentian vio- let for three minutes, washing out in water, drying, and mounting in Canada balsam. The gentian violet must be so diluted as to be nearly trans- parent. Y east can similarly be stained by magenta or methyl- ene-blue solution (two per cent.). If the latter is used, the preparation requires washing out in water. Sarcinae can hardly be said to have any pathological sig- nificance, according to Oppler (“ Miinchen. med. Wochenschr.,” 1894, No. 29). They are found in ectasias, occurring on a non- malignant basis, and in very atonic conditions; also in acute and- chronic gastritis, in ulcer, in the gastric neuroses, and the gastrop- toses ; in the last-named conditions the presence of sarcinae is rather the exception than the rule. Riegel agrees with Oppler in the assertion that sarcinae are very rarely found in gastric carcinoma. They are generally observed in biscuit or bale-shaped groups of four, eight, and sixteen individ- ual sarcinae bunched together; their occurrence as single individ- uals is seen rarely. The Oppler-Boas bacillus (Oppler, “ Zur Kenntniss d. Magenin- halts bei Carcinoma Ventriculi,’’ “ Deutsche med. Wochenschr.," 130 BACTERIA OF THE STOMACH. 1895, No. 5) is an unusually long and non-motile bacterium, which was observed in many cases of gastric carcinoma. (See Fig. 19.) In twenty cases of carcinoma Kaufmann found these bacilli nineteen times, and, according to his investigations, they have the power of abundantly forming lactic acid from various kinds of sugar. In the only case of the twenty just mentioned in which the Oppler- Boas bacillus was absent, the lactic acid was absent also. According to Schlesinger and Kaufmann (“ Wiener klinische Rundschau,” 1895, No. 15), the presence of a large number of these bacilli in the stomach contents is an indication of carcinoma, and their absence is of similar significance to the absence of lactic acid. If a stenosis of the pylorus is present, then the absence of these bacilli is an argument against carcinoma. Riegel (loc. cit.) confirms the occurrence of these bacilli in enormous numbers in carcinoma, and adds that, although there are numerous fungi that have the property of forming lactic acid in stomach contents, this can not alter the significance of the Kaufmann and Schlesinger observation. He does not consider this organism as pathognomonic of gastric cancer, but as very important for the diagnosis. Since the publi- cation of the first edition of this work, the writer and his clinical assistants have examined fifty cases of gastric carcinoma particu- larly for the Oppler-Boas bacillus. They were found in every case but one. We examined also eighteen cases of gastric ulcer without discovering this organism in a single case, and consider this examination an indispensable adjunct to every gastric analysis. Our knowledge concerning the bacteria occurring in normal and pathological stomach contents is very incomplete as yet. It ap- pears, however, that in all pathological processes we are not con- fronted with qualitatively new bacteria, but with excessive multi- plication of those normally present. The disturbances produced by abnormal augmentation of bacteria in the stomach are ex- plained by Minkowski (“ Ueber d. Gahrung im Magen,” Mit- theilung a. d. Med. Klin. Konigsberg,” edited by B. Naunyn, Leipsic, 1888, p. 156) in the following manner: 1. Substances may be formed which irritate the mucosa and pro- voke catarrhal inflammation. 2. Gas may be formed in considerable quantities, causing dis- tress by distention, and increase the mechanical insufficiency already present. 3. The fermentation may give rise to toxins. 4. Putrefaction of albuminous bodies may produce alkaline MUCUS — BILE BLOOD — PUS. I 3 I bodies that will neutralize the hydrochloric acid or what little of it may yet be secreted. 5. Gastric fermentations may have a detrimental influence on the intestinal functions. Examination of Stomach Contents for Mucus, Saliva, Bile, Duodenal Secretions, Blood, and Pus. — The presence of mucus is evident to the naked eye by its stringy and tenacious character. Mucus from the pharynx is distinguished from gastric mucus by its occurring in clumps and being discolored by dust-particles. The chemical demonstration is carried out by dissolving the mucus in liquor potassae, in which it is slightly soluble, and from which it can be reprecipitated by acetic acid. When pharyngitis, laryngitis, and bronchitis can be excluded, large quantities of mucus in stom- ach contents are indicative of gastritis. The normal stomach does not secrete much mucus. Statements repeatedly made to the con- trary can only be explained by faulty clinical observation. Mucus is dissolved or digested by gastric juice, but requires twice as long as albumin for its solution (Schmidt, “ Deutsch. Arch. f. klin. Med.,” Bd. lvii, S. 72). Gastric mucus may occur in two forms : (i) As a glassy, swollen, transparent mass ; (2) in forms of fibers or shreds. These states of mucus are to a large extent conditioned by the amount of HC1 secreted. When there is deficiency or absence of HC1, the mucus swells up. When HC1 secretion is normal or in- creased, the mucus may be increased also, but if so, it occurs in forms of fibers, strings, or shreds. The quantity of mucus is inversely proportional to the quantity of HC1 secreted ; the largest amounts are found with total absence of HC1. Microscopical exami- nation of the mucus yields unsatisfactory results ; when it contains pigmented alveolar epithelia, it is derived from the respiratory passages. Pavement epithelium suggests its origin from the mouth and pharynx, but if the gastric juice be capable of digesting, one finds only nuclei, and if it be devoid of digestive power, entire cells are found. The spiral or snail cells, first described by Ja- worski, are products of the action of HC1 on mucus, and have no diagnostic significance. If the gastric contents consist largely of saliva , this can be demonstrated by the potassium sulphocyanate, KCNS, which is a normal constituent of healthy saliva. Potassium sulphocyanate gives a dark, purplish-red color upon the addition of a solution of chlorid of iron. Bile } if present to any considerable extent, is noticeable at once 132 ANALYSIS OF STOMACH CONTENTS. to the naked eye by the compound greenish-yellow tinge it im- parts to stomach contents. Very slight amounts of bile and duodenal secretions are occasionally observed under normal con- ditions, particularly if the stomach be washed out early in the morning before breakfast, for there is no absolute closure of the pylorus when the stomach is empty. Boas has, however, pointed out that constant presence of very evident admixture of bile and duodenal secretions points to stenosis of the descending portion of the duodenum (Boas, “ Deutsche med. Wochenschr.,” 1791, No. 28., “ Ueber die Stenose des Duodenum.”). As a rule, it will be necessary to assure one’s self of the presence of bile by the Gmelin test, or the demonstration of bile acids or cho- lesterin. Gmelin’s test is carried out by adding twenty drops of fuming nitric acid to ten c.c. of officinal nitric acid in a test-tube. Ten c.c. of stomach filtrate are drawn into a pipet, and, holding the test- tube with the HN 0 3 in the left hand in a slanting, horizontal position, the filtrate is allowed to flow slowly from the pipet held in the right hand over the nitric acid. If the stomach contents contain bile, there will be formed several characteristic rings of color, which, going from above downward, are (1) green, (2) blue, (3) violet, and (4) red, but only the green color is an evidence of the presence of bile. Better results are obtained by using a conical glass on a broad foot instead of a test-tube. In the clinical laboratory they are of sixty to seventy-nine c.c., or about two ounces, in capacity. It is of some advantage to be able to place them alternately on and in front of a white and black background during the reaction. First, twenty c.c. of gastric juice, if necessary previously filtered, are placed in the glass, then ten c.c. of nitric acid added by a pipet, which is carefully carried to the bottom of the vessel ; here the nitric acid is very gradually permitted to escape by diminishing the pressure of the finger on the end of the pipet. In this manner it is easier to get the nitric acid under the gastric juice. The display of the colors, yellow, green, blue, violet, and red, occurs from above downward ; the green color is the only one that is characteristic of bile elements. The demonstration of the bile acids is affected by first precipitat- ing all albuminous bodies by boiling or by alcohol; a few drops of a solution of cane-sugar are added, and then, drop by drop, pure concentrated sulphuric acid. If the solution is now heated, a beauti- BLOOD IN GASTRIC CONTENTS. 1 33 ful purple-red color is obtained, between 6o° and 70° C. (Petten- kofer). The presence of duodenal secretions is demonstrated by testing the stomach contents for the specific ferment activity of trypsin, amylopsin, and steapsin. (See pp. 56 and 57.) Pus. — Pus is rarely found in the gastric contents, but if so, purulent inflammations in the mouth, tonsils, pharynx, retronasal fossae, larynx, and bronchi must be excluded before assigning its cause to the stomach. In one case in which we found pus in the stomach it came from an ozena ; in another it was traced to a tuberculous softening in the left lung. The significance of pus will be considered in connection with acute simple and with phlegmon- ous gastritis. Test for Blood in Stomach Contents. — Although blood may be present in the material drawn by a stomach-tube, or in vomit, it is not always easy to decide whether it was derived from the lungs or from the stomach. Vomiting may produce a cough, and, vice versa, coughing may lead to an attack of vomiting ; and in cases where either organ is liable to hemorrhage, as in tuberculous patients with a congestive state of the gastric mucosa, it is, except in rare instances, impossible to decide the origin of the blood. In cases with copious arterial gastric hemorrhage, the blood is bright red and clotted. A slower but still quite profuse hemorrhage generally shows as a black clot or mass of black clots. In very slow but continuous hemorrhage the blood collects, and may be partially digested or decomposed in the stomach before it is vomited as a black, coffee-ground material. The diagnosis of blood in the vomit is not always easily made. There are four methods of determining the presence of blood, and by one or more of them it may generally be accomplished. The first is by the microscopical demonstration of the red blood- corpuscles. In cases of suspected ulcer, all vomited matter should be microscopically examined, even when blood is not evident to the naked eye. The second is known as the guaiacum test. Two or three drops of freshly prepared tincture of guaiacum are added to five c.c. of stomach contents in a test-tube, and ozonized ether poured on the surface ; if blood is present, a blue color develops where the two liquids meet. Equal parts of tincture of guaiacum and turpentine that have been exposed to the air may be used instead of ether. This test for blood is fallacious, as almost any carbohydrate, bile, 134 ANALYSIS OF STOMACH CONTENTS. or saliva will produce the same color in the total absence of blood. The guaiacum test, which was originally proposed by Almen and Van Deen, becomes more reliable when executed by an im- proved method suggested by H. Weber. A considerable quantity of the filtrate is extracted or mixed with water; glacial acetic acid, to the amount of one-third of the entire quantity of water and fil- trate mixture, must be added. Of this acid extract about ten c.c. are poured off after settling ; then ten drops of tincture of guaiacum and twenty to thirty drops of turpentine are added. If blood is present, the mixture becomes violet-blue ; in case blood is absent, the color will be red-brown. The blue coloring-matter that indicates blood can be extracted by shaking the mixture with chloroform. Coffee-ground vomit will not permit of the correct finding of blood with either of the two preceding tests. This kind of vomit may have to be differentiated from genuine tea or coffee vomit, or from bile, by Gmelin’s test. In this form of vomit the corpuscles are disintegrated and the hemoglobin trans- formed into insoluble hematin. Still, there are two ways left to diagnose the blbod present, if any : first, the formation of crystals of hemin, and, secondly, the demonstration of the presence of iron. 1. Preparation of hemin crystals : Three to four drops of the thick sediment is mixed on a glass slide with a little common salt, then one to two drops of glacial acetic acid are added, and the mixture carefully heated over a small flame of a spirit-lamp or a Bunsen burner until bubbles begin to form. If blood is present, on exam- ining the preparation with the microscope reddish-brown, oblong crystals of hemin hydrochlorate will be recognized; their color, form, and occurrence are characteristic. This test may fail in cases where blood is present. 2. Demonstration of the presence of iron : Naturally, the patient whose stomach contents are to be examined must not have been taking iron in any form, nor any raw meats. Demonstration of the Presence of Iron in the Stomach Con- tents or in Vomited Matter. — In case one is dealing with coffee- ground material this test may become necessary. Some of the black sediment is placed in a porcelain dish, and a few crystals of potassium chlorate and two to three drops of strong hydrochloric acid are added. On heating over a flame and adding a few drops of a five per cent, solution of potassium ferrocyanid, 4KCN, Fe(CN) 2 + H 2 0 , FRAGMENTS OF MUCOSA, ETC., IN GASTRIC CONTENTS. 1 35 Prussian blue will be formed. Boas and Sidney Martin consider this a very delicate test. The Prussian blue, upon the occurrence of which this test depends, is a complex cyanid of iron, 4Fe(CN) 3 . 3 Fe(CN) 2 . Spectroscopic Examination of Stomach Contents for Blood. — A spectroscopic examination is possible when the red blood- corpuscles have become dissolved, and the filtrate of gastric con- tents contains oxyhemoglobin. The compound of oxygen with hemoglobin is distinguished by two absorption bands in the spec- trum, which occur between the Fraunhofer lines D and E in the yellow and green. If after the recognition of these lines a reducing agent is added to the solution of oxyhemoglobin, — for instance, if it is shaken with ammonium sulphid, — the two bands observed be- fore fuse into a single broad band, occupying the space between the two distinct and separate bands, or move beyond D toward the red of the spectrum. (Compare Eichhorst, loc. cit., p. 523 ; also Richard C. Cabot, “ Clinical Examination of the Blood,” Wm. Wood & Co., Publishers, New York, 1897, and von Jaksch, loc. cit.) Examination of Portions of Mucosa or Tissue Found in the Wash-water and Vomited Matter. — In the wash-water from almost every stomach, also in the samples of test-meals gained by the Ewald expression method, and in vomited matter, small portions of the superficial mucosa of the stomach can frequently be found on careful searching. Stimulated by reading the accompanying literature, particularly the work of Hayem, Boas, Einhorn, and Cohnheim, we have during the last three years made a study of such tiny bits of mucosa. To detect them more easily, the stomach is best washed in the morning, before breakfast, with 500 c.c. of warm water, which is poured into a shallow papier-mache or hard-rubber dish, the bot- tom of which is colored white and black like a checker-board ; on this background the tiny bits of tissue from the mucosa, or from any neoplasm that may be in the stomach, can be more easily recognized. These particles are usually of a reddish color; they may seem at times colorless, so that in a glass or pitcher they may be overlooked, while on the dark, flat dish they are quite apparent. These fragments come from very superficial erosions, which are pos- sibly caused by very slight local congestions or by traumatism (Ewald, loc. cit.). It is conceivable that the contractions of the muscularis of the stomach may, if sufficiently powerful, effect an arrest of the flow of 36 ANALYSIS OF STOMACH CONTENTS. circulation in the folds and cause intense congestion of the veins and capillaries, which may give rise to small hemorrhages into the mucosa. These hemorrhagic areas are very poorly nourished by the blood-current, and may eventually succumb to the autodigestive action of the gastric juice; other gastric contractions then loosen, and cast off these tiny spots of necrosis (Hartung, loc. cit .). According to Virchow (loc. cit), circulatory derangements of the larger vessels of the stomach, — the acute and chronic gastritis espe- cially, — if accompanied with vomiting and colicky contractions, are the cause of ulcers and erosions. Small erosions represent only the superficial stratum of the mucosa, generally only the vestibule or alveolus and the first third of the gland-ducts ; the entire lower half of the mucous membrane is rarely cast off (Gerhardt, loc. cit). The gland-duct remaining shows nothing pathological. At the sides and edges of the sequestrated portion the glands become longer, and the first ones that are intact usually curve themselves over the defect, partly covering it. Recovery takes place by the simple after-growth of the remaining portions of the glands. In three stomachs which were taken immediately after death (not later than two hours after), we observed what was undoubt- edly a superficial epithelial sequestrum resting loosely upon the mucous membrane in many places of what we had every reason to believe was a perfectly normal stomach. The autodigestion in this case had been prevented by pouring ninety per cent, alcohol into the organ about fifteen minutes after death. In places, portions of mucosa half as large as a lentil-seed could be dislodged by a gentle stream of water from a wash-bottle. The erosions included the inner third of the gland-duct proper (“inneres Schaltstiick ” of Stohr), and it seems that even before they were dislodged the process of repair had already begun ; for underneath small areas of necrosed superficial epithelium that were lifted from the true glandular stratum by a thin layer of lymph containing few red blood-corpuscles, cell proliferation was going on in the parietal or oxyntic cells, and in the cylindrical cells of the adjoining intact epithelium formation of mitosis and karyokinetic figures were evident in picrocarmin and eosin stains of these sequestrations of mucosa. The presence of mitosis in an apparently healthy stomach somewhat weakens the assumption (Lubarsch) that this is a valu- able sign of carcinoma. It seems possible that a process of exfoliation is constantly going on in the lining membrane of the gastro-intestinal tract, just as in ETIOLOGY OF EROSIONS. 1 37 the epidermis. It is not conceivable that the constant and con- tinuous impact and friction of the ingesta should go on daily without causing necrosis of epithelium in places. If we should hold the normal acid chyme in the palm of our hands for three or four hours three times or more every day, we would very soon notice dermatitis and exfoliations of the epidermis. In the digestive tract (for it occurs all along the small intestine) this exfoliation goes deeper than in our hands because of imme- diate autodigestion of the exfoliated spot. Although we have examined fifty human stomachs with especial regard for this phenomenon, we have failed to detect evidence of this process in minute areas in but four cases, and in these the examination was limited to a very small portion of the stomach. Even in stomachs obtained within one hour after death, and preserved by pouring alcohol or solutions of formalin into the organ, these erosions can be seen in places. We generally request a strip which begins in the esophagus, runs through the cardia, saccus caecus, entire greater curvature, and pylorus, and has a piece of duodenum attached to it. This is hardened, and in many places pieces are excised half an inch apart and embedded in cel- loidin, cut into serial sections with the revolving microtome, stained in eosin and hematoxylin and mounted in balsam. In some cases we sectioned strips running along the lesser cur- vature. In this way it was found that most of these erosions and exfolia- tions occur in the vicinity of the sphincter antri pylorici, about seven to ten cm. from the pylorus. At this point the muscu- laris has its most powerful development, and the peristalsis, and consequently the impact of the food with the mucosa, is most vigorous ; hence the epithelium here has most to suffer from fric- tion. Slight erosions can be detected in the lower part of the esophagus, where no peristalsis normally occurs but that accom- panying deglutition. So the conclusion seems justifiable that very tiny exfoliations and erosions occur in all stomachs, and, in adult life, perhaps at all times. This precludes the presumption that the pieces of mucosa are lesions produced by the stomach-tube. Boas (loc. cit.) thinks that coughing or defecation may cause the dislodgment of such loosened epithelium. When this process reaches such an exaggerated type as described by Einhorn {loc. cit., “ Erosions of the Stomach”), it is very probable that the mucosa is made less resistant by some well-developed gastric disease (one of IO I38 LITERATURE ON EXFOLIATIONS AND EROSIONS. the forms of gastritis, carcinoma, etc.), for his patients suffered from pains, emaciation, and weakness. Among the forty-six stomachs examined by myself were nineteen in which no symptoms referable to the stomach were given during life. The pieces varied from five mm. in length, and nearly as wide. Einhorn recommends intragastric spraying of a solution of 1 : 1000 of argentic nitrate for the excessive exfoliation, combined with intragastric galvanization, diet, and tonics, with a hygienic out- door life. LITERATURE ON EXFOLIATIONS AND EROSIONS OF GASTRIC MUCOSA. 1. Boas, “ Diagnostik u. Therap. d. Magenkrankh.,” “ Allg. Th.,” 3d ed., p. 220. 2. Boas, “ Ueber Gastritis Adda,” “Wiener med. Wochenschr.,” 1-11, 1895. 3. Boas, “ Beitrag zur Symptomatologie des chronischen Magenkatarrhs und der Atrophie der Magenschleimhaut,” “ Munch, med. Wochenschr.,” 41 u. 42. 4. Cohnheim, Paul, “ Die bedeut. klein. Schleimhautstiickchen f. d. Diag- nose d. Magenkrankh.,” “ Archiv f. Verdauungskrankh.,” Band 1, S. 274. 5. Cramer, “ Ueber d. Ablosung d. Magenschleimhaut durch die Sondirung,” “ Miinch. med. Wochenschr.,” p. 52, 1891. 6. Damaschino, “Note sur un nouveau procede pour l’etude de lesions de l’estomac,” “ Gaz. med.,” 1880. 7. Ebstein, “Ueber die Losung eines Stuckes d. Pylorusschleimhaut mit d. Magensonde,” “Berliner klinische Wochenschr.,” 1895. 8. Ebstein, “ Beitrage zur Lehre vom Bau der sogenannten Magenschleim- driisen,” “ Schultze’s Archiv,” Band vi, p. 530. 9. Einhorn, “ Clinical Observations on Erosions of the Stomach and Their Treatment,” “ N. Y. Medical Record,” June 23, 1894. 10. Einhorn, “State of the Gastric Mucosa in Secretory Disorders of the Stomach,” “ N. Y. Medical Record,” June 27, 1896. 11. Einhorn, “Zur Achylia Gastrica,” “Archiv f. Verdauungskrankh.,” Band 1, Heft 2. 12. Ewald, “ Klinik d. Verdauungskrankheiten,” 3d ed., p. 191. 13. Ewald, “ Ein Fall chronischer Sekretionsuntiichtigkeit des Magens ” (Anadenia ventriculi ?), “ Das Benzonapthol,” “ Berl. klinische Wochenschr.,” 26 u. 27, 1892. 14. Ewald, “ Ein Fall v. Atrophie d. Magenschleimhaut mit Verlust d. HC 1 Sekretion, Ulcus carcinomatosum duodenale,” “ Berl. klinische Wochen- schr.,” 1886. 15. Fenwick, “Ueber den Zusammenhang einiger krankhafter Zustande des Magens mit anderen Organerkrankungen,” “ Virch. Archiv,” Band 118, xil. 16. Gerhardt, D., “Virch. Archiv,” Band cxxvn, p. 85. 1 7. Hammerschlag, “ Zur Kenntniss des Magencarcinoms,” “ Wiener klinische Rundschau,” 23, 1895. 18. Hartung, O., “ Deutsche med. Wochenschr.,” No. 38, p. 847, 1890. LITERATURE ON EROSIONS. I 39 19. Hayem, “Gastritis Parenchymatosa,” “ Allg. Wien. med. Zeitung,” 1894, pp. 2-17. 20. Hayem, “ Resume de l’Anatomie Pathologique de la Gastrite Chronique,” “ Gaz. Hebdom.,’’ pp. 33, 34, 1892. 21. Jaworski u. Korcynski, “ Ueber einige bisher wenig beriicksichtigte klinische und anatomische Erscheinungen im Verlaufe des sogenannten Magenkatarrhs,” “ Archiv f. klinische Med.,” 47, p. 578. 22. Klemperer, “ Ueber die Dyspepsie der Phthisiker,” “ Berlin, klinische Wochenschr.,” 11, 1889. 23. Korcynski u. Jaworski, “ Klinische Befunde bei Ulcus u. Carcinoma Ven- triculi,” etc., “ Deutsche med. Wochenschr.,” pp. 47-49, 1 886. 24. Kupfifer, “ Epithel u. Driisen d. menschlichen Magens,” Munchen, 1883. 25. Langerhans, “ Virch. Archiv,” Band cxxiv, p. 373. 26. Meyer, “ Zur Kenntniss der sogenannten Magenatrophie,” “ Zeitschr. f. klinische Med.,” Band xvi, p. 366. 27. Rosenheim, “ Ueber atrophische Processe an der Magenschleimhaut in ihrer Beziehung zum Carcinom u. als selbstandige Erkrankung,” “ Berliner klinische Wochenschr.,” 51, 1881. 28. Sachs, “Zur Kenntniss der Magenschleimhaut in krankhaften Zustan- den,” “Archiv f. exp. Pharm. u. Pathol.,” Band xxiv, 1888. 29. Schmidt, “ Ein Fall von Magenschleimhautatrophie nebst Bemerkungen tiber die sogenannte schleimige Degeneration der Driisenzellen des Magens,” “ Deutsche med. Wochenschr.,” 19, 1895. 30. Schmidt, “ Fortgesetzte Untersuchungen iiber die Secretion des Magen- schleims,” “Deutsche med. Wochenschr.,’’ Vereinsbeilage, xm, 1895. 31. Schmidt, Adolf, “ Untersuch. iiber menschl. Magenepithel, normal u. pathol.,” “Virchow’s Archiv,” Band 143. xix. 32. Stintzing, “ Zum feineren Bau u. zur Physiologie d. Magenschleimhaut,” “ Miinchener med. Wochenschr.,” 46, 1889. 33. Stohr, “Zur Kenntniss des feineren Baues der menschlichen Magen- schleimhaut,” “ Schultz’s Archiv,” Band xx, p. 221. 34. Virchow, R., “Virch. Archiv,” Band v, p. 363. 35. Hemmeter, J. C., “ Zur Histologie d. Magendriisen b. d. Hyperaciditat,” “Archiv f. Verdauungskrankh.,” Heft 3, 1898. CHAPTER XIV. THE DIAGNOSTIC SIGNIFICANCE OF FRAGMENTS OF GASTRIC MUCOSA. One of the first to utilize these fragments for diagnostic purposes was Boas, who attributed great importance to this way of finding out the real state of the mucosa. He held that in certain con- ditions of suppressed secretion the differential diagnosis between a possible neurosis and a genuine gastritis with glandular atrophy was only possible by examination of such pieces of mucosa. 140 SIGNIFICANCE OF FRAGMENTS OF MUCOSA. Rosenheim ( loc . cit.), Boas ( loc . cit.), and Julius Friedenwald (“ Med- ical News,” June 22, 1895) emphasize the value of qualitative and quantitative testing of rennin zymogen to differentiate between chronic gastritis with glandular atrophy and carcinoma on the one hand, and nervous dyspepsia and secondary gastritis on the other. However, Ewald {loc. cit.) and also Einhorn {loc. cit.) have asserted Fig. 20. — Fragment of Mucosa showing a Normal Condition of Glands : very slight round-celled infiltration. The piece became detached above the level at which the oxyntic cells are found. X 600. that absolute deficiency of rennin zymogen is not pathognomonic of atrophy ; therefore it wmuld indeed seem as if a certain diagnosis could only be made by a small piece of mucosa. Is there any clue which can be derived from these pieces regard- ing the state of the mucosa in the secretory disorders? This we will try to answer in the following. Hayem, to whom we HISTOLOGY OF THE FRAGMENTS. 1 4 1 are indebted for the best histological investigations of the gastric mucosa, emphasizes that the individual elements of the mucosa, gland-ducts, superficial epithelium, and interstitial tissue can become diseased in a variety of ways ; the various portions of the stomach, fundus, pylorus, and cardia may exhibit different affections; and. finally, the mucosa may at different parts show different phases of disease. He distinguishes a parenchymatous and an interstitial gastritis. First, the parenchymatous : 1. Gastrite parenchymateuse hyperpeptique chloro-organique. Under this he has two sub-classes: ( a ) “D’emblee” — dyspeptic distress coming on at once — in the first stage of digestion. ( b ) “ Tardive ” — dyspeptic distress coming on in later stages — in one and one-half to two hours. Under this hyperpeptic parenchymatous gastritis, Hayem means, clinically, a hyperpepsia with hyperacidity and, anatomically, degeneration of the principal central or chief cells, with proliferation of the parietal, border, or oxyntic cells. 2. Gastrite parenchymateuse muqueuse (gastritis mucipara), by which he means a mucous degeneration, a process taking place principally in the vestibules to the gland-ducts (which are lined with columnar epithelium) and corresponds to the Sehleimkatarrli of most German writers. This is associated with hypopepsia and subacidity. 3. Gastrite parenchymateuse atrophique, which signifies, anatom- ically, the total atrophy of the glands without interstitial pro- cesses, and, clinically, anacidity or achylia. The interstitial forms he separates into two classes : (a) Those in which the round-cell infiltration; (1 b ) Those in which the sclerosis, i. e ., connective-tissue prolifera- tion, predominates. These processes are described as occurring purely as such, or mixed with forms of parenchymatous gastritis, and as leading to sub- or anacidity. In order to bring our results in critical con- sideration with those of Einhorn (loc. cit.), we have adopted his classification of the anatomical conditions found in these frag- ments. There is, however, one objection that can be urged against it, and that is the apparent fact that he has based his system upon conditions of the gland-tubes and interglandular tissue exclusively, and mentions the state of the cells only once in six types described. We shall therefore supplement his categories by adding the state and condition of the vestibular or alveolar columnar cells (Vorraumzellen), and the condition and numerical 142 SIGNIFICANCE OF FRAGMENTS OF MUCOSA. relations of the chief central or ferment cells (Hauptzellen), and the parietal, border, or oxyntic cells (Belegzellen) : I. Normal . — The gland-ducts and interglandular tissue exist in normal proportions. The columnar epithelium of the surface and of vestibule is normal, with scattered cells showing at their free ends slight mucoid metamorphosis. Average number of parietal Fig. 2i. — H ypertrophy and Proliferation of Glandular Elements. — ( From a case of per- sistent hyperacidity — specimen found in the eye of the tube after drawing test-meal .) X 500. or oxyntic cells in six ducts which were sectioned very nearly down the center = 22-40 (see Fig. 20). 2. Connective-tissue Excess . — Proliferation of connective tissue around the glands — glands and epithelial cells as in normal con- dition. 3. Proliferation of Glands . — Under this class we have in the examination of nineteen cases been impressed with the probability that there are three types of this condition : HISTOLOGICAL CONDITIONS PRESENT. 43 Type a . — Increase of gland-tubules, but normal number of border cells. In this sub-type there is a proliferation of gland- tubules. Under the same field of microscope there will be more of them than under normal conditions, since they are much closer to each other, but the number of central and oxyntic cells are from 18-42, or the same as under the normal condition. Fig. 22. — Atrophy and Vacuolization of Glandular Elements— Mucoid Degeneration of Peptic Cells — Increase of Interstitial Connective Tissue — Small Round-celled Infiltration. — ( From a case of chronic alcoholic gastritis. Found in the wash-water .) X 500. Type b . — Increase of oxyntic or parietal cells with normal number of gland-ducts. Here there seems to be no proliferation of the gland-ducts. The connective tissue and the ducts bear the same relation as in class 1, but the anilin-staining oxyntic cells maybe so increased that they lie in juxtaposition, giving the whole duct the appearance of a peptic duct of the dog; the number may reach seventy in one duct. The oxyntic cells are increased in size. 144 SIGNIFICANCE OF FRAGMENTS OF MUCOSA. Type c . — Increase of the number of ducts in which the number of oxyntic cells appear normal in size and number, and, in the same fragment or section, portions of mucosa in which the ducts are not augmented, but the oxyntic cells are increased in number and size; this third type is a combination of types a and b. When there are many oxyntic cells above the normal, the entire gland- duct assumes a tortuous or elongated shape. It seldom extends down into the mucosa in the same plane; therefore it is very rare that a section will strike down the middle of a duct. Generally the counts in sixteen ducts struck fairly along the central canaliculus are taken as an average. 4. Incipient Atrophy . — To the same field, under the micrometer, there are fewer glands present than normally ; they appear shrunken and smaller, at the same time the spaces between the glands are larger than normal owing to an increased connective-tissue forma- tion ; the latter is thickly invaded, as a rule, with small round-cell infiltration. The next type is — 5. Atrophy . — In complete atrophy there are only remnants of glands left, a few degenerated cells lying in empty circular spaces where glands had previously existed ; there is also a diffuse round-celled infiltration (see Fig. 22). 6. Vacuolization . — Round or ovoid vacuoles exist within the glands in large numbers, being the result of mucoid degeneration of some of the glandular cells ; this is generally associated with connective-tissue proliferation (see Fig. 22). Vacuoles are present in the gland-cells normally, as can be seen in the drawings of Kupher and Stohr. We have also seen them in both longitudinal and cross- section of the gland-tubules, but rarely more than two or three to the entire duct. It is conceivable that they may be produced by the process of hardening and imbedding. Some of the fragments obtained from stomachs may show characteristics of two types. Deductions from Fifty Cases. — (Hemmeter, “ Ueber die His- tologie der Magendriisen,” etc.; Boas, “Archiv f. Verdauungskrank- heiten,” Bd. iv, p. 30). In fourteen healthy persons the mucosa fragments were normal in eleven; proliferation and autodigestion marked in one, which showed also beginning small round-cell in- filtration between the ducts ; connective-tissue increase in one. In a third case the examination showed proliferation in one fragment, and a normal condition in a second found in the same wash-water. In twenty-two cases of hyperacidity the fragments of gastric mucosa found were apparently normal in four. HISTOLOGICAL CONDITIONS PRESENT. *45 Atrophy of gland-tubules and connective-tissue increase, so that there were fewer glands, — but in these few there were contained a larger number of oxyntic cells than normal, — in two cases. Proliferation of gland-ducts, with apparently normal oxyntic cells, in eight cases. Proliferation of oxyntic cells, generally without marked increase in the gland-tubules, in eight cases. In fourteen cases of anacidity or subacidity the fragment was ap- parently normal in four cases. .Proliferation of glands, with marked small round-cell infiltration, was found once. Atrophy in some form was found in the fragments from the nine remaining cases. In establishing the classification of euchlorhydria and hyperchlorhydria we could not be guided exclusively by the amount of free HC1 found after the double test-meal. Thus, a young, vigorous farmer, aged twenty-five, who never had any disease, showed on repeated examination an amount of free HC1 equal to 6o°, with a total acidity of 8o°. Ordinarily, judging simply from the analysis, such a case would be diagnosed as hyperacidity, according to the principles defined in the chapter on the normal amount of HC1 ; however, these cases can be diag- nosed justly and accurately when considered together with concomitant signs and symptoms only. Although this case had the large amount of free HC1, there was no starch indigestion, no erythrodextrin, no pyrosis; there were no symptoms referable to the stomach at all ; the man was in perfect health. Another case, a neurasthenic female had been suffering intensely from hy- peracidity and occasional gastroxynsis, and the amount of free HC1 was never over 30°. This case showed hypermotility; the stomach, as a rule, was empty twenty-five minutes after an Ewald test-meal ; with our intragastric rubber bag, in connection with the kymograph, she showed very frequent and sudden gastric peristalsis of unusual tonicity. Summary of results from examination of fragments of mucosa in fifty cases : / Perfectly normal in eleven. (a) Glandular proliferations in one ; (b) normal in one. These fragments ( a and b ) were found in same wash-water. Connective-tissue increase in two. Normal in four. Atrophy in two. Proliferation of gland-ducts, but normal oxyntic cells in eight. Proliferation or hypertrophy of oxyntic cells in eight. f Normal in four. Proliferation of glands in one. ^ Atrophy in nine. Fourteen healthy persons : Twenty-two cases of Hyper- acidity : Fourteen cases of Anacidity or Subaciditv : 146 SIGNIFICANCE OF FRAGMENTS OF MUCOSA. In general we find proliferation, therefore, present in two-thirds of these cases of hyperacidity, and atrophy in three-quarters of these cases of anacidity or subacidity. Einhorn ( loc . cit.) does not give any results from examination of perfectly healthy individuals, as his cases of euchlorhydria seem to be in patients. Of the twelve hyperacid cases, three,were normal, or very nearly so, six showed proliferation, and three showed connective-tissue proliferation. In his cases of anacidity, or, rather, what he calls achylia gastrica, of which there were seven cases, there was atrophy three times, marked vacuolization once, proliferation once, and normal condition twice. On the whole, judging from Einhorn’s results, Cohnheim’s, Hayem’s, and our own, the conclusions seem justifiable that pro- liferation of glandular elements is present in from one-half to two- thirds of the cases of hyperacidity ; and atrophy is present in from one-half to two-thirds of the cases of anacidity. Adolf 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. Our 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 we preserved the stomachs by injecting them immediately after death (within twenty minutes) with alcohol, also with formalin and sublimate, so that autodigestion was at once checked, our sections showed generally a more serious destruction of the surface epithe- lium 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 re-formed quite rapidly where the old has been lost or destroyed. In cases of suspected malignant neoplasm fragments of the growth are occasionally found and are of importance in the diag- nosis. In carcinoma of the cardia or the esophagus 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 frag- ments. Of the first wash-water in the morning, about 50OC.C. should HISTOLOGICAL CONDITIONS PRESENT. 1 47 be permitted to settle twelve hours in a conical glass such as is used for the settling of solid urinary constituents, or the gastric contents should be brought to settle out minute particles by use of the centrifuge. The sediment should be examined under a low power (about fifty diameters). The centrifuge is preferable, as long standing of the fluid causes putrefaction. Once we made the diagnosis of carcinoma when no tumor was evident, from repeatedly finding involuntary muscle-fibers when no meat had been eaten for six days after thorough lavage. Four months later, at the autopsy, it proved to be a broad, flat carcinoma of the posterior wall. The method of recognition of neoplastic fragments will be fully considered in the chapter on Carcinoma. The drawing of a longitudinal section of the secreting gland- tubules, showing beautifully the well-preserved cylindrical epithe- lium 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, inserted by a medical student who tried to aspirate, by means of the pump, a meal that had dis- agreed with him. The tearing off must have occurred in an instant, as there were no signs of inflammation in the sections. The sections were stained in a variety of ways, principally in the eosin, hematoxylin, Golgi, and Bismarck-brown stains. The minute com- munications of the oxyntic or parietal cells with the central duct are best brought out by the Golgi method (see frontispiece). The drawings of fragments found in the wash-water, illustrating glandular proliferation, with glands closely packed and connective- tissue diminished, and of glandular atrophy, mucoid degeneration, vacuolization, and small-cell infiltration, are all explained by the text accompanying the illustrations. We have seen that histologi- cal changes approaching or actually representing pathological states may be going on in perfectly healthy stomachs. Further- more, the stomachs of diseased patients may, on serial sections, show a different pathological state at different places of the mucosa. Therefore it must be borne in mind that, although the findings in hyperacidity and anacidity appear to be in some relation to the disease, this kind of investigation must not be relied upon as rep- resenting in a given fragment the condition of the entire mucosa. It represents the state of the location whence it sequestrated ; that location not being accurately known, generalizations must be made with caution. It should be emphasized that the most important conditions in 4 8 CHEMISTRY OF GASTRIC CONTENTS. these fragments are not the number of gland-ducts and the state of the connective tissue, but the relative number of oxyntic or border and chief or central cells. A fragment may show a normal or subnormal number of gland-ducts, and at the same time these may contain an abnormally large number of cells. CHAPTER XV. THE CHEMISTRY OF GASTRIC DIGESTION. Occurrence of Secretions in the Empty Stomach. — Stimulations to Secre- tions of Gastric Juice. — Significance of Foam. — Preparation of Gastric Contents. — Quantitative Analysis. — Methods. — Standard or Normal Solutions. — Indicators. — Titration. — Apparatus. * Most authors are of the opinion that no secretion is contained in the empty stomach. Schreiber (“ Arch. f. exper. Pathol, u. Phar.,” Bd. xxiv, S. 365 ; also, “ Deutsche med. Wochenschr.,” 1894, Nos. 18 to 21), however, concludes that a secretion is found also in the empty stomach ; that is, he denies a continuous secretion or gastro- succorrhea as a disease sui generis, and claims to be able to obtain 60 c.c. of a secretion possessing good digestive power from a jejune, or fasting, stomach. Pick (“ Prager med. Wochenschr.,” 1889, No. 18), who obtained similar results, believed that the secretion was set up by the stim- ulation of the tube. Rosin (“ Deutsche med. Wochenschr.,” 1888, No. 47), A. Hoffmann (“Berliner klin. Wochenschr.,” 1889, No. 12), and Martius (“ Deutsche med. Wochenschr.,” 1894, p. 638) have also obtained a digestive secretion from the fasting stomach. Although there may be found 50 to 60 c.c. of a secretion possessing digestive powers in the empty, normal stomachs of perfectly healthy individuals, this does not prove that a continued * The section on quantitative chemical analysis of gastric contents and the chapters on the condition of the blood and urine in gastric diseases and on the gases of the stomach have been written by my former 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 h’s assistance. — (J. C. H.) GASTRIC SECRETION IN THE EMPTY STOMACH. 1 49 secretion exists normally (Riegel, “ Deutsche med. Wochenschr.,” 1893, p. 735). Leo (“ Krankheiten d. Bauchorgane,” p. 54) con- siders this digestive secretion a residuum of the last previous meal, and seems to have shown conclusively that such a residuum is constantly present in the stomachs of infants after a night’s sleep (see Leo, “ Berliner klin. Wochenschr.,” 1888, No. 49). For the practical objects of diagnosis he concludes that a secretion of 50 to 60 c.c. of digestive fluid found in a fasting organ must not be considered pathological. Only when the amount gained reaches 100 to 300 c.c. does it indicate hypersecretion, which is often associated with hyperacidity (Reichmann, “ Berliner klin. Wochen- schr.,” 1887, S. 12; Bouveret [ loc . rzV.] ; Debove, and Remond, “ Les Maladies de l’Estomac ”). Riegel and Reichmann do not distinguish sufficiently between so-called 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 asserts that, with more accurate differentiation between these states, it will probably be found that the normal stomach in a fasting condition contains very little, if any, secretion. We have studied a number of 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 (“ Deutsche med. Wochenschr.,” 1894, No. 53) has experimented upon two healthy persons, before any food had been taken, and found gastric juice with hydrochloric acid in both. The amount of secretion thus obtained varied from 10 to 22 c.c. Martius (“ Deutsche med. Wochenschr.,” 1894, No. 32) and Huber “ Korrespondenzblatt f. Schweizer Aerzte,” 1894, No. 49) confirm Schreiber’s results. According to Ewald, who sums up the liter- ature (in Lubarsch and Ostertag’s “ Ergebnisse d. spez. Pathologie,” Bd. hi, 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 contain- ing free hydrochloric acid can be obtained from the fasting, or 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 swallowed saliva (Martius), rem- nants of food, pharyngeal secretion, etc., and that the state of things lies between a normal and an abnormal one, and that there is no diseased condition of the gastric mucosa. 150 MEANS OF OBTAINING GASTRIC SECRETION. In the case of typical gastrosuccorrhea, 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 quanti tatively more considerable than that found in normal jejune stom- achs. Huber compares it to a slow, gradual dying away of secre- tory irritability (“Abklingen des Sekretionsreizes ”) that has been set up by the ingesta and seems to linger after they have passed into the duodenum. 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 three per cent, solution of sodium bicarbonate to flow into the stomach. After twelve minutes this is washed out again, and should be found neutral. By thermic stimu- lation, according to Jaworski’s method, consisting of the introduc- tion of 100 c.c. of ice-water and washing it out again after ten minutes, when it should contain acid and pepsin. These methods, if successful at all, bring out the gastric juice in a most diluted state, and, therefore, give no adequate means of determining the secretion by chemical analysis. It has been claimed by Einhorn (“New York Medical Record,” November 9, 1 889) and Allen A. Jones {ibid., 1891) in this country, and Hoffmann (“ Berliner klin. Wochenschr.,” 1889, No. 13), Ewald ( loc . cit.), 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. While we have our doubts about this matter, we do not wish to imply that electricity is not a very valuable therapeutic agent in the treatment of secretory diseases; we could not, in fact, dispense with it as an auxiliary to treatment. In our opinion, the influence of electricity on secretion is doubtful. As a means of obtaining gastric secretion, this method is certainly not available. The normal secretions are best obtained by the natural stimulation of one of the test-meals, as stated in a previous chapter. Mathieu and Remond (“ Societe de Biolog.,” 1890) have pub- lished a method of determining the total quantity of stomach con- tents 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 calculated. Strauss (“ Therapeutische PREPARATION OF GASTRIC CONTENTS. 151 Monatshefte,” Miirz, 1895) has simplified this procedure, but for the practitioner it is sufficient to know the amount gained by the simple methods of drawing the contents by expression or aspira- tion. Concerning the recognition of proteid and carbohydrate in- digestion from the food-remnants, it should be added that this is much facilitated by the double test-meal used at the University of Maryland Hospital. In gastrectasias presence of foam indicates gas-fermentation. Gas may be found even in presence of normal or supernormal amount of hydrochloric acid, since F. Kuhn (“ Zeitschr. f. klin. Med.,” Bd. xxi, and “ Deutsche med. Wochenschr.,” 1892, No. 49) has demonstrated 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 mixture may be filtered and the clear filtrate subjected to analysis. The former method gives 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 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 light and air, kept indefinitely. The methods used in quantitative chemical analysis may be divided into two general classes : Gravimetric and Volumetric. The gravimetric methods consist in 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 methods, and if only a small amount of the substance in question is present it may be very difficult to separate a weighable amount. Many substances can not be separated from mixtures without losing at the same time their relation to other substances in the same solu- tion. The great objection to the gravimetric methods, however, is the large amount of costly apparatus necessary, and the length of time needed for the manipulations. 152 STANDARD SOLUTIONS. The volumetric methods are more easily performed. In these 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 solutions and empirical solutions. A normal solution is one which contains in a liter that quantity of the active reagent expressed in grams which equals the sum of the atomic weights of the constituents that combine with one atom of hydrogen. Thus the normal solution of HC 1 is a liter of distilled water containing 36.5 grams c.p. HC 1 (H = 1, Cl = 35 - 5 ) in solution. Decinormal solutions, N 10 , are one-tenth the strength of normal solutions. Centinormal solutions, N 100 , 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 under examination with standard solution in excess of that known to be required ; the excess is then ascertained by residual titration with another standard solution. In general, titration results in the formation of a compound that can readily 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 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 a watch-glass at the side. Of the above, 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 in practice the problem re- quires experience. Absolutely pure chemicals are not easily ob- tained, and such as are easily obtained, unmixed with other mineral substances, contain a variable amount of water, and are, moreover, DECINORMAL SOLUTIONS. 153 exposed to more or less danger of contamination from the impuri- ties of the air. The following methods of obtaining a tenth-normal solution are recommended as a basis for the preparation of other solutions : I. Pure, dry oxalic acid is obtained, and the crystals that show no sign of efflorescence selected. From the formula, C 2 H 2 0 4 -{- 2 H 2 0 , 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 (63 gm.) dissolved in distilled water and made up to one liter at a temper- ature of 1 5 0 C. As a tenth-normal (Ni 0 ) solution is required, one- tenth of this, or 6.3 gm., are made up to a liter as before, and used to correct the solutions employed in analysis. It must be noticed that oxalic acid in dilute solution soon decomposes; it is, therefore, to be freshly prepared as required. To prepare an equivalent solution of caustic soda (decinormal NaOH) about five gm. of caustic soda are dissolved in about 900 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 precipi- tate forms, to get rid of carbonates or sulphates. The solution 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 phenolphthalein 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 will suppose that the 25 c.c. of caustic soda solution required 28.3 c.c. of the oxalic acid solution to cause the red color to disap- pear. If 25 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 : : iooo : (X) X = 883.4 X = amount of caustic soda solution necessary for 1000 N 10 NaOH. Dilute 883.4 c.c. of the caustic soda to 1000 c.c. with dis- tilled water. After diluting the solution it should be again titrated to insure its accuracy, and, if properly standardized, it will change from red to colorless, and vice versa, by the addition of a drop or 154 INDICATORS. two of the acid or alkaline solutions, respectively. The titration should be conducted as rapidly as possible to avoid the error pro- duced by absorption of C 0 2 from the air, and the solutions kept in well-stoppered bottles for the same reason. 2. About eight gm. of pure, dry sodium carbonate are heated in a platinum crucible for ten minutes at a dull-red heat, stirring occa- sionally with a platinum wire. After heating, it is powdered in a warm mortar and allowed to cool in a desiccator. When cool, 5.3 gm. of the powder are weighed rapidly, washed into a flask with hot distilled water, and made up to a liter. This constitutes a decinormal solution of sodium carbonate. A decinormal solution of sulphuric acid is prepared in the follow- ing manner : About three c.c. of the pure acid, of a specific gravity of 1.840, is made up to about 900 c.c. The approximate solution is standardized against the sodium carbonate solution prepared as above, using a drop or two of a 0.1 per cent, 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 solu- tion 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 (No. 1). To correct this decinormal solution of sulphuric acid for very accurate work, the following method is recommended : One hun- dred c.q. of the decinormal solution of sulphuric acid is alkalinized with a strong solution of pure ammonia (ammonium hydrate). The solution is evaporated on the water-bath, heated to 105 0 C. in hot- air bath, cooled, and weighed. The amount of sulphuric acid is calculated from the amount of ammonium sulphate formed. Indicators . — An indicator is a substance used in volumetric an- alysis, which marks, 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 jthe substance under exami- nation, but in a few cases it is used outside, a drop of the solution being brought in contact with a drop of the indicator. The particular uses of the indicators will be more fully explained 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 APPARATUS. 155 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 one per cent, solution of phenol- phthalein in alcohol, colorless in acid solutions, red in alkaline solutions. It is not reliable for alkaline phosphates, bicarbonates, or ammonia. Methyl-orange solution, a 0.1 per cent, 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 alka- line carbonates. The other indicators and their uses in analysis of the gastric juice will be mentioned later. Apparatus . — The apparatus needed for volumetric work is com- paratively simple — burettes, measuring-flasks, measuring-cylinders, and pipettes. An accurate balance is required in all chemical work, delicate to a milligram and weighing up to, say, 50 gm. 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 pinch-cock, 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. The burette should be placed perfectly perpendicular, and firmly fastened. Fill by a funnel, the stem resting against the inner sur- face of the burette to avoid the formation of bubbles. Always fill above the zero mark ; gently tap the burette until the bubbles dis- appear should they be formed. Then run out a small portion (or down to the zero mark), remembering to run out enough to re- move 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. 156 TESTS FOR PRESENCE OF FREE ACIDS. CHAPTER XVI. CHEMICAL EXAMINATION OF GASTRIC JUICE. Tests for Presence of Free Acids. — Tests for Free Hydrochloric Acid. — The Dimethy l- Amido-Azo- Benzol Test. — The Resorcin Test. — Combined Hydrochloric Acid. — Lactic Acid: Formation , Significance , Detection. Reaction . — The reaction of the gastric juice, obtained by means of the stomach-tube or otherwise, after the administration of a test- meal, is always acid in the normal individual. 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 through the pylorus in sufficient quantity to neutralize 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 (NaH 2 P0 4 ), and of traces of organic acids, which occur in nearly every test- meal in quantities sufficient to produce an acidity of from six to ten degrees. Tests for Presence of Free Acids. — A delicate test for the presence of free acids is found in Congo-red. This substance occurs as a fine reddish-brown powder, dissolving readily in water to form a clear deep-red solution, which changes in the presence of free acids to a dark blue. It may be used in two ways as an indicator. 1. A solution is prepared by dissolving one gm. of the powder in ioo c.c. of water, and adding a 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 carefully TESTS FOR FREE HCl. 157 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 advantages 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. If the acidity is due to hydrochloric acid, on the contrary, the dark-blue stain on the paper changes to a lighter tint, but does not disappear 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 re- liable : 1. Dimethyl-amido-azo-benzol 0.02 pro 1000 2. Phloroglucin-vanillin 0.05 “ 3. Resorcin 0.05 “ The Dimethyl-Amido-Azo-Benzol Test. — This test, recently introduced by Topfer, is probably destined to replace all others in the clinical laboratory, both on account of its simplicity and also on account of its ready application to the direct quantitative esti- mation of the amount of free hydrochloric acid in the gastric juice. This indicator occurs in the form of a brown powder, readily solu- ble 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 per cent, 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 residue left in the receptacle in which the stomach con- tents were received. If free hydrochloric acid is present the cherry- red color develops and spreads in beautiful rings from each drop of the indicator, usually leaving in the center a clear, yellow area. 58 DIMETHYL-AMIDO-AZO-BENZOL. In case the indication is doubtful, the following modification may be employed : A small porcelain evaporating dish (or white butter plate) is thoroughly 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 background 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 acidity. It is true that in the presence of lactic acid amounting to 0.2 per cent, or more in gastric juice this test yields a red color, resembling that due to inorganic acids ; but the objection is more theoretical than real, as the presence of such an amount of organic acids seldom 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. Furthermore, the quantitative estimation of organic acidity, to be described presently, will show the necessity of employing further tests for the presence of free hydrochloric acid, on account of a specially great acidity of organic acids, which does not, as a rule, 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 gm. of phloroglucin and one gm. of vanillin are dissolved in ioo gm. of 80 per cent, alcohol. The solution must be kept in a dark- colored, well-stoppered bottle, as it soon decomposes when ex- posed to the light. The original Giinzberg formula was composed of the same amount of the ingredients dissolved in 30 c.c.of abso- lute alcohol. This solution still more readily undergoes decompo- sition, and has no advantages 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 proportion of 0.05 pro thousand 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 RESORCIN TEST FOR FREE HCl. 159 boiling 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 reagent comes only 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 gm. of resorcin (resublimed), and three gm. of cane sugar dissolved in 100 c.c. of 94 per cent, alcohol. Six drops of the filtered gas- tric juice and three drops of the solution are mixed on a porcelain plate and slowly evaporated as in the phloroglucin-vanillin (Giinz- berg) test. Care here must also 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 hydro- chloric acid be present, a fine vermilion line forms at the edge of the drops, following down the edge of the solution as evapora- tion proceeds, while the color at the periphery gradually fades, disappearing entirely after a short time, leaving a reddish-brown stain. This test has the same degree of delicacy as the phloro- glucin-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 00, 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 hydrochloric acid, it is found that a certain amount of the hydrochloric acid combines with them to form compounds which do not give the reactions of free hydrochloric acid. In other words, certain affinities of the albuminous substance must be saturated before hydrochloric acid appears in the free state. In the stomach the same reaction must take place, probably to a greater extent, due to the more com- plicated 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 hydro- chloric acid can be demonstrated. In the Ewald meal from twenty to forty minutes elapse before free hydrochloric acid can be dem- onstrated in the normal individual, while in the more complex meals considerably more time is required. This form of hydro- l6o LACTIC ACID FORMATION, ETC. chloric acid is important, inasmuch as it constitutes a part of the physiological hydrochloric acid, and stomach digestion will pro- ceed 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 be present, all these affinities must be saturated, while in its absence 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, a severe gastric catarrh, achylia gastrica, or, perhaps, cancer. From these considerations it will be seen how important the determination of the combined hydrochloric acid is,- in all conditions of anacidity. The estimation and quantitative determination of the combined hydro- chloric acid will be deferred to the paragraphs devoted to the quan- titative determination of hydrochloric acid. The amount of pure hydrochloric acid necessary to combine with ioo gm. (or ioo c.c.) of the various food-stufifs will be given in the chapter on the Therapy of HC1. 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 contents is either introduced as such in the food or is the product of abnormal fer- mentative changes in the food after ingestion. Lactic acid may be introduced in food either as sarcolactic acid 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 usually be demonstrated ; sometimes it is absent. There are cases of carcinoma 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. Traces of lactic acid can usually be detected for some time after the administration of the Ewald breakfast or similar meals, RECOGNITION OF LACTIC ACID. 1 6 1 though at the height of digestion the usual tests are negative, due either to the absorption of the lactic acid, or the interference of free hydrochloric acid, or the products of digestion with the delicacy of the tests.* In cases in which it is desirable to prove the forma- tion 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-particles 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 Uffelmann. Ten c.c. of a four per cent, solution of carbolic acid are mixed with twenty c.c. of water, and a drop of a strong solution of ferric chlorid added. A beautiful amethyst-blue color is produced, which turns a canary-yellow when treated with a solu- tion 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 peptones. Glucose, acid phosphates, citric acid, 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 results is the following: Five or ten c.c. of the filtered gastric juice are treated with ten times their 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 as above. 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 it is a good test for clinical purposes. Boas’ 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, formic acid and acetic aldehyd are formed : C 3 H 6 0 3 = CH 3 COH + HCOOH. * Sticker (“ Munch, med. Wochenschr. 1896, No. 26) has shown that passage of carbohydrates through the mouth is followed, without exception, by the formation of more or less lactic acid. 62 DETECTION OF LACTIC ACID. Acetic aldehyd may be easily recognized by its action on Ness- ler’s reagent, or upon an alkaline solution of iodin in iodid of potassium. Nessler’s reagent is prepared in the following manner: One hundred c.c. of a four per cent, solution of iodid of potas- sium are warmed, and while warm treated with iodid of mercury until a small amount remains undissolved. After cooling, 40 c.c. of water are added. Two parts of this solution are then treated with three parts of a strong solution of caustic potash ; any precipi- tate which may form is filtered off and the reagent kept in a well- stoppered bottle. The solution of iodin is prepared by mixing a solution of iodin in iodid of potassium with caustic potash or potassium carbonate. Method . — The filtered gastric juice is tested for the presence of free acids as above, and, if present, 10 or 20 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 dioxid. After cooling it is extracted with 100 c.c. of ether free from alcohol by shaking for half an hour. After stand- ing for a short time to allow separation to take place, the ethereal layer is drawn off and evaporated (avoiding a flame), the residue taken up in 45 c.c. of water, shaken, and filtered. The filtrate is treated in an Erlemeyer flask with 5 c.c. of strong sulphuric acid and as much black oxid 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 10 or 15 c.c. of Nessler’s reagent or alkaline iodin solution prepared as described. Carefully heat the flask, and if lactic acid is present aldehyd will distil over, forming aldehyd 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 iodin is employed. Butyric acid can usually be determined by its odor alone, which is that of rancid butter. In case of doubt, 10 c.c. of the gastric juice are extracted with 50 c.c. of ether, the ethereal solu- tion evaporated, and the residue taken up with water. The odor is more evident in this concentrated aqueous solution. A small amount of calcium chlorid causes the separation of an oily layer of butyric acid ; strong mineral acids also separate the oily layer or drops of the acid. QUANTITATIVE ANALYSIS OF THE STOMACH ACIDS. 1 63 Acetic acid may also be detected by its odor. Ten c.c. of the gastric juice are extracted with ether, the ether evaporated, the residue taken up with a small amount of water, accurately neutralized with caustic soda solution, and mixed with a few drops of a very dilute solution of ferric chlorid. In the presence of acetic acid this gives a dark-red color. 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 carbo- hydrates have been ingested, usually associated with an excess of lactic acid. It has been shown 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 significance is attached to the presence of acetic acid in the stomach 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 sig- nificance as the occurrence of lactic acid — viz., stenosis of the pylorus with dilatation and fermentation. CHAPTER XVII. QUANTITATIVE ANALYSIS OF THE STOMACH ACIDS. Numerous methods have been devised for the estimation of the amount of free hydrochloric acid present in the gastric juice. The most convenient method of estimation for clinical purposes is that of Topfer, which at the same time estimates the acidity due to organic acids and acid salts, and that due to the combined hydro- chloric acid. Topfer’s Method. — Three indicators are used in this method: 1. A 0.5 per cent, alcoholic solution of dimethyl-amido-azo- benzol. 64 topfer’s method. 2. A one per cent, aqueous solution of alizarin (alizarin mono- sulphonate of sodium). 3. A one per cent, alcoholic solution of phenolphthalein. 1. As has been mentioned under the head of tests for free hydro- chloric acid, dimethyl-amido-azo-benzol reacts to very faint traces of mineral acids, particularly hydrochloric, but to organic acids only when present in very large amounts, and not at all to com- bined hydrochloric acid or acid salts. It will be seen that by this indicator we can easily find the amount of free hydrochloric acid. Topfer’s method gives results as reliable as those of the improved Sjoqvist’s or Braun’s method, according to Paul Hari (“Arch. f. Verdauungskrankheiten,” Bd. it, S. 332). Ten c.c. of the filtered gastric juice are measured into a small, clean flask, and a few drops of dimethyl-amido-azo-benzol added. The solution turns a bright red in the presence of free hydrochloric acid. The solution is now titrated with a decinormal solution 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 alizarin solution added, and the solu- tion titrated with the decinormal solution of caustic soda until the solution turns to a clear violet color. As this tint is difficult for the unpractised eye to recognize, Topfer recommends the following preliminary tests: (a) To five c.c. of distilled water add two or three drops of the alizarin solution. A clear yellow color results. (1 b ) To five c.c. of a one per cent, solution of disodium phosphate add the alizarin solution as above. 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 alizarin, as above, 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 solution as a guide in the titration. 3. To a third portion (ten c.c.) of the filtered gastric juice two or three drops of phenolphthalein solution are added and the solution titrated with the decinormal solution of caustic soda. After a cer- tain 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 solution a dark-red color is produced at the point of contact, topfer’s method. 165 fading into rose color on agitation. The titration must be carried on until the entire solution has reached this color and no line of separation can be made out on adding a drop of the caustic soda solution. 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 100 c.c. of the gastric juice as that number of degrees of acidity. For example, the number of c.c. of the caustic soda solution necessary to neu- 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 23 degrees = 23 c.c. The second method of stating the results is to give the amount of acid per thousand in terms of hydrochloric acid. As each c.c. of the solution of caustic soda will neutralize 0.00365 gm. of pure hydrochloric acid, the above example would show 0.8395 gm. of hydrochloric acid per thousand, or 0.08395 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 alizarin 4.9 c.c. of the caustic soda solution were required, and (3) with phenolphthalein 7.5 c.c. of caustic soda solu- tion 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 hydro- chloric acid, the acidity referable to this is 35 degrees, or o. 12775 per cent. 2. Alizarin shows the tint of an alkaline reaction when the free hydrochloric acid, organic acids, and acid salts have been neutral- ized, 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 alizarin, the amount of acidity due to organic acids and acid salts will be found ; in this case 49 — 35 = 14 degrees, or 0.05 1 1 per cent. 3. Phenolphthalein turns to a dark-red color when all the acidi- ties of the solution have been saturated, including the combined hydrochloric acid. The amount of combined hydrochloric acid may be found by subtracting the acidity found by alizarin from that found by phenolphthalein; in this case 75 — 49 = 26 degrees, or 0.0949 per cent. l66 METHOD OF MARTIUS AND LUTTKE. Method of Martius and Luttke. — By this method the amount of physiological hydrochloric acid, the free and combined hydro- chloric acid, are found, as well as the total chlorin of the gastric juice, by determination of the amount of chlorin. The method is based upon the fact that by moderate incineration the free hydro- chloric acid can be driven off, while the chlorin in combination 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 per cent, of pure nitric acid. This solution is approximately made up by dissolving 17 gm. of pure crystallized nitrate of silver in 900 c.c. of a 25 per cent, solution of nitric acid, and adding 50 c.c. of the liquor ferri sulphur oxydati of the German Pharmacopeia (the liquor ferri oxysulphatis [“ National Formulary ”] will serve the same purpose). The solution is then standardized against the solu- tion of hydrochloric acid and diluted to the proper volume. Each c.c. of the solution is equivalent to 0.00365 gm. of pure hydro- chloric acid. 3. A decinormal solution of ammonium sulphocyanate. Eight gm. 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 chlorin present in the gastric juice, 10 c.c. of the stomach contents, after thorough mixing, are measured into a small cylinder graduated to 100 c.c., and treated with 20 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 c.c., once more agitated, and filtered through a dry filter into a dry flask. Fifty c.c. of the filtrate are then titrated with the decinormal solution of ammonium sul- phocyanate until a permanent red color appears. Multiply the number of c.c. of ammonium sulphocyanate by 2, as only half the filtrate was taken, and subtract from the number of c.c. of nitrate of silver added (20); the result will be the number of c.c. of the nitrate of silver solution precipitated by the total chlorin of the gastric juice and correspond to the same number of c.c. of deci- LEO’S METHOD. 1 67 normal solution of hydrochloric acid, the whole amount of chlorin being expressed in terms of hydrochloric acid. 2. To determine the amount of chlorin in combination with in- organic bases. Ten c.c. of the filtered gastric juice, or of the well-mixed stomach contents, are evaporated to dryness in a platinum or porcelain cru- cible, 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 ioo c.c., or until the filtrate comes away free from chlorids, which may be shown by treating with a drop of silver nitrate. If the filtrate remains perfectly clear after the addition of a drop of nitrate of silver, the residue is free from chlorids. 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 ammo- nium sulphocyanate as before. The amount of ammonium sulpho- cyanate solution subtracted from the amount of the silver solution (ten c.c.) gives the amount of silver precipitated by the chlorids re- maining 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 and combined hydrochloric acid is de- termined. Modifications . — I. By titrating with decinormal caustic soda solu- tion, using dimethyl-amido-azo-benzol as an indicator, we obtain the amount of free hydrochloric acid ; this subtracted from the sum of the free and combined hydrochloric acid together, as arrived at by the method No. 2 on previous page, will give the amount of combined hydrochloric acid. 2. By determining the total acidity with phenolphthalein and sub- tracting from it the amount of free and combined hydrochloric acid, we can estimate the acidity due to organic acids and acid salts. 3. 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 modification 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 chlorid, a neutral salt, while the acid salts are not affected. During the reaction, however, the calcium chlorid 68 QUANTITATIVE ESTIMATION OF LACTIC ACID. reacts with the phosphates to form acid calcium phosphate (mono- calcium phosphate, CaHP 0 4 ). As this requires double the amount 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 chlorid solution before titration. Method . — Ten c.c. of the gastric juice are shaken up with 50 c.c. of ether to remove organic acids. The residue after drawing off the ethereal layer is treated with five c.c. of a concentrated solu- tion of calcium chlorid and titrated with the decinormal solution of caustic soda, using phenolphthalein 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 dioxid 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 chlorid 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 platinum loop 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 considerable amount of free organic acids. Lactic Acid— Quantitative Estimation. — A simple clinical test for lactic acid has been devised by Strauss (“ Berliner klin. Woch.,” 1895, No. 37). A separating funnel is graduated to five c.c. below and twenty-five c.c. above. The funnel is filled to the five c.c. mark with gastric juice and ether added to the twenty-five c.c. 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 and the mixture treated with two drops of a solution of the officinal tincture of the chlorid of iron, diluted 1 : 10. On QUANTITATIVE ESTIMATION OF LACTIC ACID. 169 25 c.c. -5 c.c. shaking the mixture a greenish-yellow color is produced if lactic acid is present in the proportion of I per 1000 or more. If present in the proportion of from 0.5 to I per 1000, only a pale-green color is produced. Boas’ Method. — This method of esti- mating the amount of lactic acid depends upon its oxidation into aldehyd and the estimation of the latter by means of a standard solution of iodin. Solutions required : 1. A decinormal solution of iodin is prepared by dissolving twenty-five gm. of potassium iodid in about 200 c.c of water, and dissolving in this 12.6 gm. of resublimed iodin. The solution is diluted with distilled water to 1000 c.c., and requires no correction. 2. A decinormal solution of sodium arse- nite : Dissolve 16.5 gm. of sodium arsenite in about 900 c.c. of distilled water. It is then titrated against the decinormal solution of iodin and diluted so that the two solu- tions are equivalent. 3. Hydrochloric acid (sp. gr. 1018). 4. Normal solution of potassium hydrate (56 gm. 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 be absent, this addition is unnecessary) and evaporated to a syrup. A few drops of phosphoric acid are added and the solution boiled slightly to expel carbon dioxid. 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 solution ; evaporate ; take up the residue in forty-five c.c. of water, and filter. The filtrate is treated in an Erlemeyer flask with five c.c. of sulphuric acid and a small amount of manganese dioxid. 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 appa- ratus. The distillate is received in a large flask well stoppered. The mixture is distilled at a gentle heat until about four-fifths of Fig. 23.— Strauss’ Mixing Funnel for Lactic Acid Determinations, 1^0 ANALYSIS OF THE STOMACH CONTENTS. the fluid has passed over. The distillate is then treated with twenty c.c. of the decinormal solution of iodin and the same amount (twenty c.c.) of the normal potassium hydrate solution, thoroughly 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 iodin determined by titration with the solution of sodium arsenite. The sodium arsenite is added until the solution is decolorized; fresh starch solution and the iodin solution are then added until the blue color becomes per- manent. Each c.c. of the iodin solution in excess of the sodium arsenite solution is equivalent to 0.003388 gm. of lactic acid. Quantitative Estimation of Fatty Acids. — Leo (“ Centralblatt f. d. med. Wissenschaften,” 1889) has recommended the following method: The total acidity of the gastric juice is first accurately determined. Ten c.c. are boiled until the vapor given off has no longer an acid reaction. The residue is then titrated with Tor normal NaOH, using phenolphthalein as an indicator. The loss in the total acidity gives the amount of the fatty acids. This method does not give accurate results, as some HC 1 is given off in the boiling process. By determining the amount of HC 1 before and after the boiling, the amount lost is determined and correction can be made, greatly increasing the accuracy of the method (Adler). Total Organic Acids. — The total organic acids are best esti- mated by the method of Hehner-Seeman, called, by Leube, Braun’s method. Ten c.c. of the gastric juice are accurately neutralized with a decinormal solution of caustic soda, using phenolphthalein 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 car- bonate formed determined by titration with a decinormal solution of hydrochloric acid. As the presence of free carbon dioxid in- terferes 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 dioxid in solution, and the excess of acid determined by back titration with a decinormal solution of caustic soda. This method is based upon the fact that when salts of the SALIVA. 171 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 dioxid. This method is simple. Martius and Liittke speak favorably of it, and the author has confirmed its accuracy by control analyses with other methods. CHAPTER 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 stimulate the secretion, and as it forms it is placed in a clean receptacle. It is a clear, slightly opalescent fluid, of a mucoid consistency, having a specific gravity of from 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 amylo- lytic, 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 small amount of saliva. A few drops removed and treated on a testing-plate with a drop of iodin solution give the characteristic blue color of starch. After a moment or two a few drops removed will show a violet color, and by treating a portion at intervals the color changes gradually to a deep reddish brown, and finally disappears. Different products of the action of the fer- ment 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 iodin. Later the color becomes reddish brown, due to the change of the starch entirely into dex- trins and sugar. When digestion has gone on until the solution gives no color whatever with iodin, the solution still contains some form of dextrin (achroodextrin), as may be shown by the addition 1 72 TESTS FOR PTYALIN. of alcohol, 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, ac- cording to the investigations of Nasse, von Mehring, 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 constit- uents. 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 quantities as are found in the gastric juice, not only stops its action, but possibly destroys 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 normally be demonstrated in the stomach until the lapse of fifteen or twenty minutes, the greater portion of the starch is transformed into sugar and achroodextrin. Under normal condi- tions, then, we should find, in the gastric juice removed for exami- nation, sugar, achroodextrin, and a faint trace of erythrodextrin. The presence of a marked reaction of erythrodextrin may be taken as valuable presumptive evidence of hyperacidity, its ab- sence indicating either normal acidity or subacidity. Only in rare instances has absence of ptyalin from the saliva been seen. There are some unexplained cases in which, with a normal or diminished acidity, 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 amylolytic power of the salivary excretion ought always to be examined in such cases. Pepsin. — The proteolytic ferment of the gastric juice is active only in an acid medium, and is destroyed by very dilute solutions of the alkaline carbonates. Pepsin is probably not secreted as such, its precursor 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 can perform the office. Pepsin, like the other ferments, has the property of changing an almost unlimited amount of proteids, providing the products of its action are removed when formed, and the temperature kept at a favorable point, as it TESTS FOR PEPSIN. 1 73 appears to act by its presence, not being itself destroyed or changed by the reaction. While it has never been isolated in a pure state, we know that a product can be obtained by complex chemical methods which, while intensely proteolytic, exhibits none of the reactions of proteids ; so that the ferment, whatever its nature, is probably not a proteid. 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 I : 1000, 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 added 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 suffi- cient quantity to bring the acidity to two or three per thousand ; the third is acidulated as in number two and a few grains of pepsin added. The three tubes or glasses are now placed in the incubator, 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 solu- tion of the egg-albumen, the specimen contained pepsin ; if numbers two and three only show digestion, the contents contained pepsino- gen but no pepsin ; while if only the third tube or glass shows traces of digestion, the specimen contained neither pepsin nor pepsinogen. Pepsinogen. — This substance is supposed to be secreted 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 differently 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 the thermostat at a temperature of 40° C. for three hours, at the end of this time noting the presence or ab- sence of signs of digestion. The test proposed by Hammerschlag for the peptonizing power 174 DETECTION OF RENNIN. of the gastric juice has been highly recommended in the recent works on gastric diseases. It is carried out in the following manner : A solution of about one per cent, of albumen containing 0.4 per cent, free hydrochloric acid is prepared, and ten c.c. added to each of two tubes. To one, the control-tube, five c.c. of dis- tilled water, to the other five c.c. of the gastric juice, are added, and both tubes set in the incubator for one hour at body-temperature. At the end of this time the amount of albumen in each tube is estimated by the Esbach albuminometer, the difference between the two tubes showing the amount of digested albumen. Two objections may be brought against this method : (1) The Esbach albuminometer is by no means an accurate method of esti- mating the amount of albumen ; (2) peptones are, in part if not completely, precipitated by picric acid in the cold. Boas, following out the observations of Brficke (“ Vorlesungen fiber Physiologie,” p.311, 1884: Quantitative Determination of Pepsin, etc.), 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 per 1000), so that the tubes contain the gastric juice in dilutions of 1 : 10 and 1 : 20. To each tube a small flake of egg-white or fibrin is added and put in a thermostat at the temperature of the body. From the amount of dilution at which digestion ceases, an idea may be gained of the amount of pepsin or pepsinogen which any gastric juice contains. For comparison, similar tubes may be prepared of normal gastric juice, and the digestive power of the two compared. Chymosin or Rennin and Rennin Zymogen. — In addition to pepsin, the gastric juice also contains a ferment, or its zymogen, whose special property appears to be the precipitation of casein from milk. As in the transformation of pepsinogen into pepsin hydrochloric acid is required, so rennin zymogen in the gastric juice is not transformed into rennin except in the presence of hydrochloric acid. Certain neutral salts of lime, such as calcium chlorid, however, have the power of transforming rennin zymogen into rennin, even in neutral or slightly alkaline solutions. The following tests for the presence of rennin and its zymogen have been devised by Boas : Rennin . — Five c.c. of the gastric juice are exactly neutralized with a decinormal solution of caustic soda, five c.c. of neutral milk TEST FOR RENNIN ZYMOGEN. 175 added, and the mixture, after being well shaken, is placed in an incubator at the body-temperature. If rennin be present, the casein will form a firm coagulum in from ten to fifteen minutes. A relative quantitative estimation of the rennin 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, i : io, I : 20, etc. To five c.c. of each of these dilutions five c.c. of neutral milk are added, and the tubes placed in the thermostat at the body-temper- ature for fifteen minutes. At the end of this time the tubes are removed and the dilution at which no coagulation takes place is noted. In stating the dilution note must be taken of the fluid added in neutralizing. Rennin Zymogen . — Five c.c. of the gastric juice are rendered faintly alkaline by the addition of a decinormal solution of caustic soda ; one c.c. of a one per cent, solution of calcium chlorid and five c.c. of neutral milk are added. The tube is placed in the ther- mostat, and after fifteen minutes should show a firm cake of casein if rennin zymogen be present. Quantitative . — The gastric juice is rendered faintly alkaline by adding a decinormal solution of caustic soda and dilutions pre- pared, i : io, i : 20, etc., estimating in the dilution the amount of fluid added in alkalinizing. Five c.c. of each of these dilutions are placed in test-tubes with five c.c. of neutral h milk and one c.c. of a one per cent, solution of calcium chlorid. These are placed in a thermostat at the body-temperature, and at the end of fifteen minutes the dilution at which the enzyme fails to act is noted. From the observations of Boas and others it appears that the secretion of the ferments and the pro-enzymes is less affected by the minor disturbances which may cause a temporary arrest of the acid secretion of the stomach. Decrease in the activity of the ferments, on the other hand, is usually the result of some organic change in the gastric mucosa. By experiment upon normal individuals it has been found that rennin is active in dilutions of from i : 30 to 1 : 40, and rennin zymogen in dilutions varying from 1 : 100 to 1 : 150. It has been found that, even in the absence of free hydrochloric acid, the fer- ments may be active up to the limit observed in normal individuals, and that in such cases the condition of anacidity was a temporary matter, due to some mental or circulatory disturbance, the acid re- appearing when the cause of the disturbance was removed. I76 PRODUCTS OF PEPSIN DIGESTION. On the other hand, in cases of anacidity in which the rennin 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 a quantitative investigation of the gastric ferments is from the prog- nostic standpoint. Action of Pepsin on Proteids. — The action of pepsin upon proteids only takes place to a slight extent in a neutral solution. Faust (“ Zur Kentniss des Pferdeblutserumalbumins,” u. s. w. ; “Archiv f. experiment. Pathol, u. Pharmakol.,” Bd. xli) has shown that crystallized serum-albumin, when treated with a neutralized extract of the gastric mucous membrane, gives off to the fluid a small amount of a highly nitrogenous neutral body, possibly a cyanamid. In acid solution the action is a very complex one and not as yet fully understood. The first observable result of the action of a hydrochloric acid solution of pepsin upon a coagulated albumen, 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 appearance. The egg-white then begins to dissolve, as is shown by the presence in the solution of a substance precipitated by neutralization, which may be called syntonin, or acid-albumin. This action takes place also in acid solutions to which pepsin has not been added. The next step is one in which the pepsin plays an important part. The syntonin or acid-albumin is changed first into the primary albumoses, proto- and hetero-albumose. These undergo further change and become deutero-albumoses, and, finally, peptones. These substances may be distinguished from each other by the following reactions : [a) Native albumins may be removed from the solution, if pres- ent, by rendering the stomach contents faintly acid, if not already so, and boiling. The precipitate will consist of the native proteids, viz., albumin and globulin. (£) The solution is carefully neutralized by the addition of a weak caustic soda solution. The precipitate will consist of syntonin or acid-albumin. The neutralization must be exact, as the precip- itate is dissolved by an excess of acid or alkali to form acid-albu- min or alkali-albumin, respectively. ( c ) The filtrate from which the albumin and acid-albumin has been removed is now saturated with magnesium sulphate and fil- tered. The precipitate, which consists of the primary albumoses, proto- and hetero-albumoses, is dissolved in water, placed in a SEPARATION OF ALBUMOSES. 1 7 7 dialyzer, and the salts removed by dialysis. As hetero-albumose is insoluble in pure water, it is precipitated by the removal of the salts, as in a dialyzer. 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-albumin, 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 washed thoroughly with a saturated solution of ammonium sulphate. The precipitate is redissolved in the least amount of water pos- sible, faintly acidulated with acetic acid and saturated with common salt, which precipitates the primary albumoses, leaving the deutero- albumose, or secondary albumose, in solution. After filtration the secondary albumose may be detected by saturating again with ammonium sulphate any precipitate which may form consisting of deutero-albumose. It may be detected also by adding a consider- able amount of common salt to its solution and acidulating with nitric acid. A precipitate will form in the presence of deutero- albumose, 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 a few drops of a very dilute solution of copper sulphate. If peptones are present in the solution a pink or rose-red color appears. Under some circumstances the precipitation of the albumoses by ammonium sulphate is incomplete, and in these cases the method given by Muller (“ Zeit. f. phys. Chemie,” Bd. xxvi, S. 48) gives good results. The stomach contents are treated with an equal volume of a thirty percent, solution of ferric chlorid, nearly neutralized by the addition of a solution of caustic soda and filtered. The filtrate is treated with a small amount of zinc carbonate, well shaken and again filtered. The filtrate is clear and colorless, and may now be tested by the biuret reaction as given above. 7 § GASTROSCOPY. CHAPTER XIX. GASTROSCOPY. Although the method and instruments for directly inspecting the interior of the stomach are by no means perfect, the author has considered it practical to insert this account of the procedure because of its undoubted future development as a diagnostic aid. The first one to use a gastroscope was Mikulicz (“ Ueber Gas- troskopie u. Oesophagoskopie,” “Wien. med. Presse,” 1 88 1 , No. 43 ; also “ Wien. med. Wochenschr.,” 1883, Nos. 23 and 24). The instrument used was made by Leiter, of Wien, and was curved at an obtuse angle. The following account of the technic and value of the method is quoted from Rosenheim (loc. cit .) : “ Gastroscopy is founded on the fact discovered by this author, that in the majority of cases (eighty percent.) it is possible to in- troduce, without special difficulty, a straight, rigid tube, twelve mm. in diameter, the patient having first been placed in the dorsal posi- tion. It is possible to introduce such a tube far into the stomach, often as far as the navel, and eventually below the same. The establishment of this fact first furnished him with a foundation on which gastroscopy could be developed, after he had come to the conclusion that an optical apparatus, to be suitable for the stomach, must be straight as in the cystoscope ” (Rosenheim, “ Gastroskopie,” “ Berlin, klin. Wochenschr.,” 1896, No. 13). Apart from complications that are due to tumors, exudations, enlargement of the liver, etc; (that is, to the pathological-anatomical conditions), apart also from congenital anomalies (abnormally con- torted course of the esophagus or abnormal contraction), two facts are to be considered in the light of an impediment to a successful probing by means of introducing a rigid tube into the stomach : In the first place, the bend to the left, or spiral twist, which the esophagus shows so frequently in its subphrenic part; and, secondly, the occurrence of spasm at the lower physiological contraction of the organ. With continued practice it becomes apparent that the anatomical obstruction, caused by the change in the direction of the esophagus, may usually be overcome if the instrument is intro- duced from the right angle of the mouth, preferably while the head is turned slightly to the right, laterally. DESCRIPTION OF GASTROSCOPE. 179 The obstruction before the cardia, caused by spasm of the muscles of the esophagus, can not be eliminated mechanically ; here the man- ner of introducing the tube makes no difference, and soothing the patient, persistence, and adaptation can alone lead to the desired result. Local anesthesia is useless. How much the occurrence of the spasm is due to the psychic condition of the patient was shown by numerous observations with invalids, particularly neurasthenic persons, who were timid and restive when the probe was first introduced, and with whom it was impossible to penetrate to the stomach ; while later, after they had become familiar with the proceeding, this was easily accomplished. It is necessary to keep in mind, also, that the spasm appears more frequently with persons who are suffering with an ulcer or carcinoma near the cardia. Description of the Instrument. — (See Fig. 24.) The gastroscope is a straight metal instrument, 68 cm. in length, 12 mm. in diameter, consisting of three concentric systems of tubes, and terminating in a larger head piece for the different conduits. The inner tube (1) forms an optical apparatus, the ocular of which is situated at 0, and a rectangular prism, P, is located in front of its objective lenses. The visual angle of the telescope (otherwise constructed according to the principle which has been approved in the cysto- scope, viz., as a terrestrial telescope) amounts to 6o°, so that it is possible to inspect an area five cm. in diameter at a distance of five cm. from the object. The center of the portion in view lies i8o GASTROSCOPY. vertically over the small side (cathetus) of the rectangular prism which receives the image. In order to inspect a surface the center of which does not lie at right angles over the cathetus, the rectangular prism may be replaced by an acute angular prism ; by this means those surfaces also can be examined that are situated above, which can be only partially viewed by means of a rectangular prism. The absolute necessity of inspecting parts of the stomach which appear at varying heights — for instance, the region of the pylorus — explains this arrangement. The optical apparatus is inclosed by a tube (3) that is closed at the lower end by a head-piece, A , carrying a tip of rubber, G. Just above the tip there is an aperture, E f which is closed by a glass window, behind which there is situated an incandescent lamp, as shown in 5 . At the upper and lower ends of the lamp the metal contacts that conduct the current are fastened. Above the window there is a second aperture, B, in which the prism is adjusted, and inside of which it may even be moved up or down. In the tube (3) there are four canals separated from one another. Two of these canals, which end at C and D , serve to conduct water through the instrument and around the lamp, to prevent excessive heating of the tubes caused by the incandescent lamp. The third canal is used to receive the wires that conduct the current to the lamp; while the fourth canal, which begins at / and opens at the lower end of the instrument behind the window, E, is used to introduce air, which must be pumped into the stomach, by means of a blast, to distend its walls. Toward the top the thin tube terminates in a larger head-piece that establishes tlffe connection of the canals with the different conduits for water, air, and elec- tricity. Figure 24 (1) shows the sliding tube, a tube with a centimeter scale, that can be shoved over the instrument (3) and easily re- volved on the same. It has an aperture at E corresponding to the aperture B, and, by being turned 180 degrees, it serves to cover this aperture, as well as the prism lying behind the same, so as to prevent the optical apparatus from being soiled by mucus while the instrument is being introduced. If the external tube is so adjusted that the aperture B is closed, and if, to further protect the optical apparatus, the latter is turned 180 degrees so that the exposed surface of the prism faces the side of the tube, then the prism enjoys a double protection, and in consequence the instru- ment can not be soiled while being introduced. Small metal knobs DESCRIPTION OF GASTROSCOPE. 1 8 1 are attached to the top of all three tubes, to enable us to control from the outside their position in the stomach ; when these stand in a straight line the observer knows that the prism is not covered by the revolving tube, but faces the cavity of the stomach through the aperture. The electric current -f - and — is introduced at the points of contact by means of a movable cable that is equipped with an interrupter. The intensity of the electric current is six- teen volts. In conducting water through the apparatus a stand carrying an irrigator is used. The two rubber tubes conduct the water through the instrument. By means of a cock the flow of the water can be interrupted. Another tube carries the water that has passed through the instrument into the w r ater-bucket. To cool the instrument it is advisable to use, not cold water, but water of about 40° C., in order that the lenses of the optical apparatus and the surfaces of the prism may not be covered with a film of moisture caused by sudden condensation. The stand carries the accumulator (storage battery) used to furnish the elec- tricity ; this is supplied with a rheostat for regulating the current, and also with an interrupter. It is absolutely necessary in every case to convince ourselves, before carrying out the gastroscopic investigation, that the way from the teeth, as far as the great curvature, is really unobstructed, and no special difficulties are offered to the passage of a straight rigid tube while the patient occupies the dorsal position. This test should never be neglected. At the same time the procedure should be carried out with the greatest caution. Rosenheim employs for this purpose a hollow steel probe seventy cm. long, and having the diameter of the gastroscope (12 mm.), or a smaller one, ending likewise below in a rubber appendage, in the side of which there is a small aperture provided with a blast ; the parts can be screwed off to facilitate cleansing; a centimeter scale is engraved on the sides. This probe is introduced in the dorsal position, preferably from the right corner of the mouth; after measurements along the back have been made to determine the distance of the cardia from the teeth, and after having applied a four per cent, solution of cocaine to the pharynx, the patient is directed to breathe quietly and deeply, and to lift his right hand on feeling a pain in the region of the stomach or above the same. If the patient shows pain, the procedure must cease at once. If resistance is felt, a moment of rest intervenes, or eventually the I 82 PROCEDURE OF GASTROSCOPY. instrument is retracted a little, only to try again whether the resist- ance yields under gentle pressure, the reaction on the part of the patient meanwhile determining the degree of energy that is to be employed in this manipulation. The absolute law in probing is to avoid all strong pressure, otherwise lesions of the membrane, even perforation of the esophagus or stomach, may be the consequence. After the diaphragm has been passed, air is pumped into the stomach and we determine how far the instrument is able to pene- trate into the inflated organ. The correct guiding of the instrument from the right corner of the mouth plays an important part in the success of introducing the instrument in the majority of cases. If we wish to get our bearings and inform ourselves by means of the telescope about the vast cavity of the stomach, it is prefer- able to start from the normal position just described : The point of the instrument far down at the great curvature, the window turned to the front. In this position the front wall of the stomach approaches the eye closely, within from two to three cm., so that we see it magnified. A hasty glance suffices to recognize the condition of the mucous membrane here, and we then immediately change the position of the instrument by revolving it slowly to the right so that the prism faces the pylorus. This part of the stomach and the adjoining portion of the small curvature vary in their distance from the prism in various cases. The distance is from six to twelve cm., and the image which we receive of this section is, therefore, usually somewhat reduced in size (to about one-half). We now are examining a part of the organ that, from a practical point of view, is perhaps the most important, since ulcers and cancers are so frequently located there. We exert ourselves now, starting from the opening of the pylorus, to investigate systematically the whole hollow cone, situated to the right. This part does not escape us, as a rule, if we move the tube gradually from the great curvature upward while revolving the apparatus generally in both directions. After we have found the orifice of the stomach, as a fixed point, it is not difficult to espy from the same the neighboring section of the small curvature, at least, and something of the rear wall. The higher the portio pylorica lies behind the liver, the more it (as is normal) bends away to the rear on the right, the more difficult it is to inspect, while a low position greatly facilitates our investigation. In the former case (for which we may be somewhat prepared by the preceding inflation of the stomach) the optical apparatus pro- THE ESOPHAGOSCOPE. 183 vided with an acute-angled prism is recommended. It is possible to recognize how .different the distance is between the prism and the pylorus during the normal position of this segment of the organ and during dislocation of the same. In the former case the distance is more considerable ; we must withdraw the instrument farther, to bring at least a part of the portio pylorica within the Fig. 25. 1. Esophagoscope. 2. Obturator. 3. Esophageal forceps. 4. Esophageal applicator. {Rosenheim.*) angle of the prism ; and if the point of the instrument diverges a little farther to the left from the vertebral column, this approach to the cardia avails nothing ; under all circumstances we receive only an image of the part beneath the orifice of the stomach. During * Our thanks are due to Professor Theod. Rosenheim (Berlin) for presentation of these illustrations. 8 4 GASTROSCOPY. these manipulations we are in danger of being surprised by an obscuring of the field of vision, since we are compelled to approach closely the descending part of the small curvature adjoining the cardia. These disturbances are avoided if we take a view of the pyloric portion from a deeper point, a thing which can be conve- niently effected by the employment of an acute-angled prism in the apparatus; the center of the circle, which we then survey, no longer stands perpendicularly over the prism. We no longer re- ceive the image from a region at the same level with the prism, but from one a little higher. If the pyloric portion is dislocated to the lower margin of the liver, or deeper, the rectangular prism opposite the same can easily be adjusted without needing a correction. After inspecting the pyloric portion we approach the great curva- ture with the point of the gastroscope, and turn the instrument to the left by 180 degrees; while slowly withdrawing the instrument, we next inspect the part of the fundus and cardiac portion that belong to the left half of the body. The investigation is now com- pleted ; the illumination is discontinued, the revolving tube is pushed in front of the window, the blast is removed in order that the gases may quickly escape ; only after this is the instrument withdrawn. Rosenheim has devised a gastroscope more recently in which the stream of water for the cooling of the electric lamp is dispensed with ; the lamp is only flashed now and then, and not kept incandescent continuously. The latter instrument is thinner and only ten mm. in diameter. Conclusion. — (i) Not all parts of the interior of the stomach can be inspected. Portions of the greater curvature — of the pos- terior wall, the immediate neighborhood of the cardia — are not visible. It can not be practised on all individuals. (2) All suspected cases of ulcer must be excluded if recent pain and hemorrhages have occurred. Ulcers at pylorus are less liable to be injured than those near the cardia. (3) Rosenheim suggests that gastroscopy may be employed for the early diagnosis of carcinoma and its differentiation from ulcer. It is an inconvenient procedure and very difficult of execution, and not free from danger. PART SECOND. THERAPY AND MATERIA MEDICA OF STOMACH DISEASES. CHAPTER I. THE PRINCIPLES OF DIETETIC TREATMENT OF GASTRIC DISEASES. In the chapter on the Physiology of Digestion we have briefly considered the various food-substances, their nutritious and innu- tritious constituents, the amounts of each, requisite to maintain a healthy organism, and their caloric values, etc. It is one of the far-reaching deserts of the great Father of Medicine to have first methodically developed dietetics for the sick as a special discipline and an integral part of therapy. In his classical dissertation on the conduct of febrile diseases (Hippocrates, “ De victus ratione in morbis acutis ”), in his aphor- isms, and in many other treatises, he emphasizes the great impor- tance of careful regulation of nutrition for patients. His principles, based upon analytical experience, are stated with unsurpassable precision. His dietetics are free from speculation, and regard the nature and stage of the disease, the constitution, age, and habits of the patient ; above all, they show what is in our days termed an in- dividualizing principle. It would seem probable that a therapeutic aid that had been logically considered at the very dawn of medical knowledge, and by such an able mind, would at the present time be one of the most highly developed in medicine, particularly when one reflects upon the declaration of Donders (“Die Nahrungsstoffe des Menschen,” Crefeld, 1853): “Whoever works at the develop- ment of our knowledge on food-substances is working on a broad basis for the development of mankind.” Fortunately for us, many bright intellects have already applied themselves to this work, and 13 185 86 DIETETIC TREATMENT OF GASTRIC DISEASES. our knowledge has been enriched by treasures of valuable informa- tion. But the well-advised special student can not fail to recognize that we have only entered a vast territory, and that the greater part of it remains to be explored. Even the small portion which by hard toiling is clearly our own is, we regret to say, far from being the common property of the profession — at least, it does not seem to be taken advantage of ; the profession at large failing to realize that a logical and individualizing diet is a more potent therapeutic factor than medicine. The results so far obtained show great domains of research and inquiry yet to be explored for truth bearing on dietetics. And many of our present results demand reconsideration for correct interpretation. Various eminently fitted observers disagree on vital dietetic questions, because the special point of view from which each one’s research (“ Fragestellung ”) was undertaken was not identical, sometimes not defined with precision. Sometimes the intricacy of the question to be solved did not permit of direct methods of investigation, and indirect methods had to be em- ployed. The scales of digestibility of various foods, as devised by Leube and Penzoldt, for instance, were arrived at by determination of the time which the stomach required to discharge these foods into the duodenum. Evidently the term “digestibility” means the rate of solution of the various food-substances by the constituents of the gastric juice, or of the intestinal juices, as the case may be. Diges- tibility, therefore, has reference mostly to secretion, but the rate of the gastric expulsion of chyme is a problem of motility. To be of easy digestibility food-substances must — 1. Offer only a slight resistance to the digestive juices — i. e. y they must be of easy solubility. 2. They must not impede or accelerate peristalsis. 3. They must not excessively irritate the digestive organs, either mechanically or chemically. 4. They must not increase the processes of fermentation or putrefaction. 5. The greater portions of the substance must be absorbable either in the stomach or intestines. To say that veal in amounts of 100 gm. leaves the stomach in one to two hours does not imply that it is digestible, for the same may be said of sawdust (from actual experiment of a colleague, made upon himself). By our method of duodenal intubation we CRITERION OF DIGESTIBILITY. ! 8 7 succeeded in regaining from the duodenum 56.4 per cent, of a weighed amount of ingested veal two hours and fifteen minutes after, it had been eaten. The veal was weighed and was easily recognizable ; besides, nothing else had been eaten at the time. The celerity with which a food disappears from the stomach, there- fore, is not so much an indication of its digestibility as it is of the gastric motor power. A more correct way to determine the digestibility of various foods — one which we have systematically experimented with on a number of volunteers from our classes who had a normal digestion — is to find out how much by weight of a known amount of in- gested food is converted into peptone or dextrose and maltose, as the case may be, in a given time — for instance, one hour or thirty minutes. In a large number of these experiments we aspirated some of the weighed test-meals from the duodenum (method of the author, Boas’ “Archives for Digestive Diseases,” vol. 11). For approxi- mately accurate results it is sufficient to weigh the insoluble residue of the particular food that is drawn out of the stomach. It is necessary to have those experiments which are to serve as crucial tests of digestibility made with comparatively pure proteids, such as meat and egg, and pure carbohydrates, such as rice. The amount of water used in the cooking and the amount ingested must be known, and can be found out by evaporating control samples to dryness. It may thus be learned how much proteid is rendered soluble by the pepsin hydrochloric acid, how much casein is digested, or how much of starch is converted into dextrose and maltose in the fifteen to forty-five minutes, or any desired period during which the par- ticular ferments are permitted to act. The results can naturally not be absolutely correct, but only relatively so ; at least, they are more nearly correct than the conditions of the experiment will allow the results of Leube and Penzoldt to be. The absolute amount of food need not be regained ; all that is re- quired for a comparative study is to learn in a given sample — say, thirty c.c. — the proportion of soluble and insoluble chyme. Dex- trose present can be determined by titration, as we have shown else- where ; and from the reactions of the various transition products from proteid to peptone the amount of the latter can also be approximately known, particularly if the amount of solid residue of proteid that can be regained is learned first. 1 88 DIETETIC TREATMENT OF GASTRIC DISEASES. It is an interesting fact that the results of these tests of digesti- bility performed directly on the normal stomach can be confirmed by control analysis, made with animals (making allowance for the increased secretion of HC1 in dogs), and by analysis made with artificial digestive mixtures in the incubator. In the chapter on Digestion by Pepsin it has been explained why the exact gastric digestion can not be imitated in a test-tube, mainly because the formation of peptone in the stomach remains at a certain percent- age by the absorption of peptones over that amount. As soon as the amount of peptone exceeds a certain percentage it retards, and may even suspend, proteolysis. The retardation of proteolysis which occurs in hyperacidity may be explained in this way — i. e., more peptone is formed in a given time than normally, and as it can not be absorbed as rapidly as it is formed, it inhibits further proteolysis by its presence ; besides, the stomach attempts to main- tain a fairly constant degree of concentration of contents by removal of chyme into the duodenum. Notwithstanding all these differences, test-tube or artificial diges- tion experiments are very valuable for comparative studies in digestibility, particularly when deductions are made in combination with test-meals on the normal and diseased human stomach. In the stomach, we must bear in mind, there is a carbohydrate and a proteid digestion ; we can, however, rarely give food exclusively from the standpoint of gastric digestion, for Leube and Penzoldt’s tables show that the greater portion of the digestive work is exe- cuted in the intestine. Our results, so far as we can judge at present, agree with the main ones of these observers. Leube studied the duration of reten- tion of various foods in the stomachs of diseased patients, and Penzoldt in the stomachs of healthy individuals (that is, before they were expelled in the duodenum). We have confirmed their princi- ples by experiments, ascertaining the amounts of proteid and carbo- hydrates converted into a soluble form in a given time in normal and pathological stomachs. These experiments were supported by tests made with artificial digestive mixtures and on dogs. The explanation of the agreement of these various methods of testing digestibility is probably the fact that food-substances which are most rapidly and thoroughly converted into a soluble form are also most easily expelled into the intestines. Easily soluble proteids, though solid, are readily converted into a liquid or at least semisolid form, in which they are readily propelled onward. ADAPTATION OF DIET. I 89 Proteid soluble with difficulty is retained longer, because the pre- antral sphincter has, to a degree, a selective action, and will not readily permit the passage of solid food. The matters of solu- tion and rate of propulsion of foods are, then, the factors which are intimately correlated and largely go to make up the quality of digestibility. The definition of a digestible food, then, is one that makes relatively small demands upon the secretory and motor functions of the stomach, which is readily absorbed and produces no subjective complaints or feeling of discomfort. From a pathological point of view, however, the conception of digestibility is a variable one. Foods that maybe easily digestible for a gastric-ulcer patient may be very indigestible for a case of atrophic gastritis or of cancer. Leube and Penzoldt’s method of estimating gastric digestibility by the rate at which various foods are expelled into the duodenum, gives a relatively correct indica- tion for the sound normal organ, because secretory and motor functions are equally taxed as they go hand in hand. The results can not be unconditionally applied to abnormal states where one or the other function, or both, are disturbed, sometimes in opposite directions, secretion increased, motility diminished, or vice versa. There are conditions in which gastric digestion is com- pletely destroyed and must be replaced by the intestinal function. There are states of absolute and permanent loss of gastric secre- tion (achylia), in which the propulsion of food from the stomach is not delayed. Now, one can not speak of gastric digestibility in these cases, because there is very little, if any; but such cases may have a perfect intestinal digestion, so that the distinction between “ gastric ” and “ intestinal digestibility ” is important. The diet of patients must be varied and adapted to the con- dition of the gastric secretion, motility, and absorption ; but it must also — and this is generally overlooked — be adapted to the sensibility of the stomach. The neuroses of sensation, considered in the clinical portion of this work, offer a fertile field of work to the thoughtful dietarian. An abnormally increased feeling of hunger, in which this intensely heightened sensation can hardly be appeased by food and absence of the feeling of satiation , — bulimia and akoria , — as well as absence of hunger, in which the appetite is very readily appeased, can in many cases be successfully treated by diet. By treating bulimia dietetically, we do not mean to suggest unlimited ingestion of food, but rather a painstaking investigation I9O DIETETIC TREATMENT OF GASTRIC DISEASES. of the cause, which may be an unduly large stomach or conval- escence from infectious disease (typhoid). We do not class the increased desire for food observed in men performing exceptional physical work, in women during pregnancy and lactation, as well as in rapidly growing children, as bulimia. This augmentation of hunger is due to a greater requirement of food, because the organ- ism has greater expenses in supplying material for growth or energy. Many forms, perhaps sixty per cent., of bulimia cases are due either to hyperesthesia, hyperacidity, or hypermotility. If these are causes, the treatment given under these diseases should be administered (clinical part). The meals should be allowed every two or three hours, and consist largely of such proteids as have a great combining affinity for HC1. These are given under Flei- scher’s list of the HC1 binding power of foods. But if an irritative state of the glandular layer can be ascertained, the diet should be largely amylaceous. If the motility be exaggerated with the hyper- acidity, it is well to direct the patient to drink frequently of cold alkaline waters, such as the Saratoga Vichy, or the alkaline effer- vescent water recommended by Jaworski (see clinical part), particu- larly when the stomach is empty. Anorexia , in its severe forms, is most often due to organic changes in the gastric walls. In the nervous forms it is often benefited by a course of forced feeding with the stomach-tube. Persistent anorexia in highly neuropathic individuals had, in fact, best be treated this way as soon as the patients positively refuse food, because a complete cure can frequently be accomplished by gavage alone. The feeding through the tube has a moral and educational effect not to be underestimated. In my experience as physician-in-charge of Bay View Asylum, many cases were observed to resume taking their meals with good appetite as soon as they became convinced that forced feeding would be insisted upon. But aside from this moral effect there is also a physiological one : this consists in the supplying of a stimulant to the stomach in the form of food. Nourishment is the proper stimulant to secretion, and if it is wanting for a long time the functions of the stomach soon become arrested, and with them the appetite. The nutritive stimulant to the gastric mucosa is food; it causes a filling of the blood- and lymph-vessels, thus indirectly bringing about a better nutrition of the histological elements of the mucosa and a resump- tion of HC1 formation with ferments, which in anorexia is, as a rule, suppressed. In fact, as appetite causes eating in the healthy, so EFFECT OF ABSORPTION ON SELECTION OF DIET. I9I eating will cause appetite in these cases of anorexia. In mild cases of anorexia a sensation of hunger is frequently started up by salty and “ piquante ” articles, such as caviar, sardelles, herrings, etc., and at the same time small doses of alcohol with bitter tonics, such as the Angostura bitters, are advisable. The extractive substances in fresh meats (bouillon) are stimulants to appetite (Pawlow). Lavage with solutions of chlorid of sodium or a .04 per thousand HC1 is most effective. The most essential condition to a proper dietetic treatment is, of course, that the patient should have appetite. A great point is gained if he can be made to take food with pleasure. For the management of those cases with anorexia we must refer to the article on this subject. The author agrees with Sir William H. Broadbent (“ Brit. Med. Jour.,” vol. 11, 1893, p. 1268) when he says: “ In all cases in which the cause has been overfeeding or improper food, or food taken at a wrong time, an extremely strict and meager diet for a few days will be the best treatment. No advantage is gained, however, from a low diet in neurotic cases. “ The object we set before ourselves must be, not to level down the diet to the digestive capabilities of the stomach, but to level up the digestion till it can deal efficiently with the amount of food for the due support of the nervous system. No hard and fast rule can be laid down. Speaking generally, such a (neurotic) patient will digest food which he relishes better, even if it have the repu- tation of being indigestible, than the most digestible and scientific- ally prepared food which he eats by order, and dislikes. A very common experience is that he is tempted by a good dinner, eats largely and indiscriminately, and then, instead of a bad night and great discomfort, which he thinks he has deserved, he sleeps well and feels all the better for his indiscretion.” A very important point will be to disabuse the patient’s mind of the idea that pain after meals necessarily indicates that the food has been unsuitable. One day, and under one set of circumstances, anything will agree ; on another day, under different circumstances, nothing is digested. Directions must be given not to eat when exhausted or excited or anxious, not to jump from meals and rush off to work of any kind, and to eat very slowly. The state of the gastric absorption has to be considered in the selection of a diet. In most text-books this factor of dietetics is entirely neglected. In the light of the most modern knowledge on absorption, that furnished by the work of von Mehring, according I92 DIETETIC TREATMENT OF GASTRIC DISEASES. to which it is almost limited to cane-, grape-, and milk-sugar, maltose, dextrin, alcohol, and peptone, while water is not at all absorbed (see Absorption), it is not at once evident why the state of absorption should be considered in selecting a diet. Von Mehring’s results, however, seem to point the way in selecting peptones, maltose, dextrin, alcohol, etc., where we must depend on rapid diffusion of nutritious material, and also in avoiding water, or foods containing water, where the gastric walls are weak, because it is not absorbed and overdistends by its weight. Not only this, but simultaneously with resorption a more or less active excretion of water occurs into the stomach. The amount of this excretion of water increases or diminishes with the quantity of substances resorbed or taken up. Certain gastric diseases con- nected with much fermentation are supposed to be in etiological relation with tonic muscular spasms — forms of tetany of gastric origin. Bouveret and Devic (“ Rech. clin. et experim. sur la tetanie d’origine gastrique,” “Revue de Med.,” 1892, xn, p. 48) assert that alcohol is instrumental in favoring the formation of an intragastric diffusable toxin in dilations and hypersecretive states, and that these poisons bring about the spasms. Fleiner (loc. cit.) and Kussmaul recommend that no alcohol in any form be given in dilatations with pyloric stenosis, where naturally the absorption of the alcohol must be very much retarded. The latter authors do not accept the toxic origin of the spasms, but suggest that the alcohol causes a tremendous excretion of water into the stomach, thus robbing the organism of a requisite amount, — a tetany, there- fore, due to drying of muscles and nerves ; both views are merely hypotheses. The practical deduction is that where the absorption has been found defective by tests, alcohol had best be avoided. •Boas recommends that explicit written directions be given to each patient after the diagnosis has been made, concerning — 1. Exact time of meals. 2. An exhaustive account of articles of diet and luxury that are allowed.* 3. An exact statement of the weights and measurements of the foods and beverages. 4. Brief instructions on the preparation of the food, temperature of drinks, seasoning, etc. 5. Special account of foods that are forbidden. * Dr. E. R. Schreiner has devised a useful diet-list by which the physician is enabled to rapidly fulfil this desideratum. (Published by P. Blakiston’s Son & Co., Phila.). PREPARATION OF FOOD. 193 The time for the ingestion of food is an essential factor in dietetics, particularly with our American business men, with whom it is a common practice to sacrifice meal hours to business. The hours for meals should be religiously observed by gastric sufferers, and the hours for stomach-rest or fasting also. Hyperacidity and forms of nervous dyspepsias occasionally require small meals frequently repeated ; the same is true of some types of atonic and stenotic gastrectasias, where the chyme still reaches the duodenum but with difficulty. Other stomach diseases require long pauses of rest between the meals, and it is not always possible to state a priori how much digestive work and how much rest any particularly diseased stomach may require. It is only after a prolonged study of the various gastric functions that the physician can give correct instruction in chronic cases (see chapter on the Use and Abuse of Rest, etc.). There is much need for enlarging the dietetic menu of dys- peptics; nothing should be forbidden, except there are actual facts founded on experiment, the nature of the disease, or the idio- syncrasies of the case proving it to be harmful. Our experience is that when the menu is too limited a certain disgust for the diet eventually becomes manifest, resulting either in temporary anorexia or a disregard of the directions and indulgence in for- bidden foods. Directions as to preparations of the food are sometimes neces- sary. Here the physician must be able to indicate, for instance in an- or subacidity or atrophic gastritis, that the meats should be finely scraped or cut, then cooked in a steam broiler, with a liberal season- ing of pepper and salt. In hyperacidity, gastroxynsis, gastritis acida, and the convalescence from gastric ulcer, all seasoning except a little salt must be avoided; wherever there is excess of HC1 the meats should also be finely divided before cooking. The amounts of paprika, red and black pepper, mustard, horse-radish, lemon, vinegar, and ginger, that can be allowed in cases of absolute sup- pression of secretion (as these materials have some effect in stimu- lating secretion), must be stated. The preparation of soups and gravies, the amounts and kinds of fats and sugars to be used in the cooking, are points of importance. For a more detailed account of these indispensable methods and directions for preparations of food, reference must be had to works on Dietetics , — vide Gilman Thompson, Munk and Ufifelmann, Wiel (“ Tisch fur Magenkranke ”), Boas (“ Diat u. Wegweiser f. Magen- 194 DIETETIC TREATMENT OF GASTRIC DISEASES. kranke ”), Woltering (“ Diatetisches Handbuch ”), Yeo (“ Food and Diet ”), Penzoldt (vol. iv of the “ Handbuch f. spezielle Therapie ”), Honigmann (“ Zeitschr. f. Krankenpflege,” 1894, No. 8), Wegele (“ Diatetische Behandl. d. Magen- u. Darmkrankh.”), Leyden (“ Ernahrungstherapie u. Diatetik Moritz (“ Die Krankenernah- rung,” Universal-Lexikon der Kochkunst, 2 vols., published by J. J. Weber, Leipzig).* The Diet as Influenced by the State of the Secretion.— The anomalies of secretion are: (1) Hyperacidity, (2) Sub- and Ana- cidity, which form one group of gastric neuroses. In another group we may classify hypersecretion (of normal gastric juice in which the HC 1 is not increased or diminished). This is the “ Magensaftfluss ” of Reichmann, the gastrosuccorrhea chronica or periodica, of which Schreiber holds that it is not a disease sui generis. We class the so-called “ gastroxynsis ” of Rossbach with the hypersecretions, because it impresses us to be a gastric neuro- sis with excessive secretion and hemicrania, and is hardly entitled to be classed as a distinct and separate disease. As far as diet is concerned, 3 the hypersecretions do not exactly coincide with the hyperacidity in the treatment. For the augmented gastric juice in the super- or hypersecretions may be a passive act on the part of the glands, — their activity may be kept up by retained food. But in hyperacidity the excessively high percentage of HC 1 is an active process, an irritative state of the mucosa in which it responds with excessive formation of acid to all food stimuli. In the hypersecretions the diet should be selected with regard to favoring rapid gastric evacuation. In hyperacidity there is no better treatment than rest. These are states in which there is an accelerated digestion of albuminous and proteid foods, and a retardation of carbohydrate digestion, which is caused by an inhibition of the inverting action of the diastase of the saliva, the ptyalin by the excessive amount of HC 1 . The same is true of the pancreas diastase. Boas has shown (loc. cit.) that a neutralization of the chyme will restore the diastatic action, but we have assured ourselves that if the gastric acidity has once reached 0.3 per cent, the action of the ptyalin can not again be so perfectly restored by neutralization with sodium carbonate as it was before. In other words, excessive hyperacidity permanently damages the ptyalin. * A Complete Encyclopsedia on the Art of Cooking, Preserving, Table Ethics, Menus, etc. DIET IN HYPERACIDITY AND HYPERSECRETION. 1 95 It may resume some inverting action after neutralization, but it is not equal to that evinced during the first forty-five minutes of normal gastric digestion. An intensely acid gastric juice will pro- duce a deleterious effect on the bile by precipitating from it a sub- stance up to the present time not isolated, by which the bile aids in partial digestion of the fats. In a similar way the secretion of the pancreas is prevented from performing its work, because it can do so only in an alkaline or faintly acid medium. There are three organic diseases which dietetically come under this group of ex- cessive acidity or secretion ; these are ulcer, gastritis acida, and ulcus carcinomatosum. Concerning the dietetic treatment of hy- peracidities, uniformity of opinion does not exist. As a general rule, it can be stated that in the simple forms a bland, unirritating diet, which at the same time binds as much hydrochloric acid as possible, should be prescribed. We favor a diet that does not irritate the mucosa any more than is absolutely necessary. There are two indications : (i) An etiological one, directed to the condition of the mucosa and demanding rest for the irritative state present ; ( 2 ) a symptomatic one, directed to neutralization of the excess of HC1 by diet having the greatest HCl-binding affinity. These two indications are to some extent opposed to one another. The etiological indication necessitates avoidance of albuminous food, for in our experience proteid and albuminous foods produce an increased secretion of HC1. The second or symptomatic indication calls for a large ingestion of albumen to combine with the HC1. In case of ulcer the food must be the least irritating, the mildest that our menu contains. Not the total quantity of acid secreted constitutes hyperacidity, but the amount secreted in excess of what is required for combining with the proteids. For instance, a case may show hyperacidity after a simple Ewald test-breakfast of a roll and a glass of water, because the acid secreted meets with nothing to combine with and remains free, while the same case may show very little excess or normal acidity after the first of our double test-meals, as employed at the University of Maryland, consisting of beefsteak, eggs, rice, milk, and bread, because the acid, in this in- stance, at once enters into combination. The more abundant secretion of HC1 is more completely used up when the meals con- sist of a preponderance of proteid food than when they con- sist of carbohydrates. Therefore, the dietetics of these cases, as usually recommended, include the red meats, venison, game, turkey, eggs, chocolate, etc., liberally, a certain limitation of carbo- I96 DIETETIC TREATMENT OF GASTRIC DISEASES. hydrates, and the alkaline carbonated waters. In hyperacidity and supersecretion spices are to be forbidden, and only so much salt as is indispensable to make the food palatable. All acids, such as vinegar or lemon-juice, in the food simply aggravate the trouble. There are undoubtedly different kinds of hyperacidities. We feel justified in distinguishing two classes: (1) Those in which there is a preponderance of nervous symptoms and fragments of the mucosa show no increase in the number of gland-tubules or in the oxyntic or acid cells ; these cases are, then, of a purely neurotic type. (2) Secondly, those in which there is an increase in the number of gland-tubules or in the oxyntic cells. A simple neurotic case may eventually lead to increase of oxyntic cells, by the greater demand for acid secretion. There is no hard and fast line to sepa- rate these classes, but they demand somewhat different treatment for reasons stated further on. A number of competent observers have recommended an exclusion of proteid and an increase of the carbohydrate foods in hyperacidity. For, although proteid foods combine with more HC 1 than any other, they are also the greatest stimulants to the secretion of acid. See Dujardin-Beaumetz (“Traitement des maladies de l’estomac ”) and von Sohlern (“ Berlin, klin. Wochenschr.,” xci, Nos. 20 and 21) ; Fleiner (“ Volkmann’s klin. Vortr.,” No. 103) ; Rummo (“ Terapia clin.,” 1892, Nos. 10, II, 12); v. Jaksch (“ Zeitschr. f. klin. Med.,” Bd. xvii, 1896). These writers argue that carbohydrate food is not so irritating and calls forth much less secretion of HC 1 . W. Roux (“ Entwicklungsmechanik der Organismen,” 1895) states that increased activity heightens the specific force of the organs, while diminished activity lowers it. The existence of the cells of the organism depends upon their work ; those that work most are nourished best and grow strongest. In other words, the elements in any tissue that are incited to greatest activity and function will gain supremacy over others and increase in strength and numbers. The deductions are not purely theoretical, for not only do we find proliferation of acid cells in hyperchlorhydria to be present in from fifty to seventy-five per cent, of the cases, but in animals with a high acidity of HC 1 (dog, fox, wolf, etc., carnivora) there is a tremendous multiplication of acid cells. It seems logical, therefore, that there are cases in which the hyperacidity may, in the long run, be kept up by a proteid diet, although for the time being this diet may HYPERACIDITY TREATED BY AMYLACEOUS DIET. 1 97 render the acidity less by combining with the free HC 1 . Ex- perience teaches that the most annoying symptoms, the gastralgia and pyrosis, are promptly relieved by the proteid diet, and we shall indorse the latter as most eminently proper in selected cases. When, however, the symptoms are relieved only very briefly, par- ticularly when the ratio of the ethereal to the preformed sulphates in the urine is found to become very high under a rich albuminous diet, and the indican increases, we advise a diet rich in carbohy- drates and fats. The author has analyzed the gastric contents of two men who were vegetarians by principle, the average amount of free HC 1 in one being 12.5 after an Ewald test breakfast; in the other the average amount of free HC 1 was 10.6. In a Japanese student who had lived, according to his own statement, almost exclusively on rice, milk, sugar, and a kind of Japanese bread, the average amount of free HCi after an Ewald test breakfast was 14.6. See Chas. E. Simon, on “ The Relation of Indican to Gastric Diseases” (“ Amer. Jour. Med. Sciences,” August, 1895). This can be filled by all breads and articles made from flour, rice, peas, beans, potatoes, the cereals, oatmeal, and rich milk and butter. It is true that in some forms of hyperacidity these substances can be found sometimes six hours after they are ingested, unchanged in the stomach ; but here the motility is seriously at fault. As alkalies must be given even with a proteid diet, they should, in case the food consists largely of carbohydrates and fats, be given imme- diately after meals and, if need be, combined with ptyalin or diastase to hasten amylolysis. It is frequently observed, that the amount of free HCI becomes less and less, and the alkalies and artificial ferments may be dispensed with if the amylaceous diet is persisted in. This diet we suggest particularly after the albuminous diet has failed, for there are cases of hyperacidity which are undoubt- edly maintained by an exclusive proteid diet. It must not be over- looked that such a thing as a pure carbohydrate diet does not exist, because all articles of this class contain protein, and some very considerable quantities of it ; peas, beans, and lentils, for example, contain more protein in the percentage composition than pork, beef, ham, or fish. It is not a total exclusion, but simply a re- duction of proteid that is practically recommended. According to Pawlow (“ Die Arbeit der Verdauungsdriisen,” p. 187), fats and oils inhibit the secretion of HCI by the gastric mucosa. We have tested this on ten normal persons and ten cases of hyperacidity and could confirm the observation, so that we now recommend I98 DIETETIC TREATMENT OF GASTRIC DISEASES. butter and olive oil in as large quantities as can be expediently eaten, for cases of hyperacidity. Strauss, of Berlin, has found that sugars as in candies reduce the secretion of HC1. All cases of hyperacidity require a certain amount of carbohy- drates. It is a matter of experience that proteid diet alone will not permanently satisfy their cravings. Flour and the many arti- cles prepared from it are not readily converted into dextrin in an excessively acid medium. It is expedient, therefore, to recommend dextrinized flours, such as Avenacia, Maggi, and Kufifeke’s flour. The American product, “ Horlick’s Food,” is a flour in which the wheat starch has been almost entirely converted into dextrin by malt diastase. It has a high caloric value, and its price is sufficiently moderate for humbler practice when artificial flours seem indi- cated. Regarding the preparation of carbohydrates, we refer to the special lists given in the text under the various diseases, and to Wegele’s “ Diatetische Kiiche.” In the hyperacidity of ulcer the diet must be of the least irritating quality, and the coarse-fibered meats — beef, mutton, lamb, veal, venison — are not to be allowed, even during the periods of convalescence, and when they are finally conceded, they should all be reduced to a pulpy (scraped) form. In sub- or anacidity, when the motor function is good, the prob- lem of diet is not so complicated, because the deficient HC1 can be supplied if it is found necessary, and the intactness of the peris- talsis insures a good intestinal digestion. ^ As the motility is the only safeguard against malnutrition, great care should be taken to avoid injuring it by overloading the organ. Small meals frequently repeated are indicated, consisting of very tender meat (in fine sub- division), soft, tender vegetables, such as finely chopped spinach, cauliflower, ends of asparagus, puree of potatoes, peas, beans, len- tils. \ The fats, which are best given in form of rich cream and good butter, have a high caloric value. Unfortunately, they depress the already deficient secretion of HC1 still more in subacidity. They must be forbidden as soon as it is discovered that they cause gastric irritation by formation of fatty acids. The diet must vary according to the cause of the sub- or anacidity. If it can be ascertained that there is no injury of the glandular apparatus, but simply an inhibition of secretion, the salty and spicy articles, even pepper and ginger, may be advised. Such sub- or anacidities are improved by taking caviar, sardelles, DIETETIC PREPARATIONS OF BEEF. I 99 small pickled herrings, or anchovies, before meals, because salt is an approved stimulant to secretion. In these cases HC 1 is not only supplied because of its deficiency, but also because it is actually curative in hastening the resumption of secretion. If, however, the absence of HC 1 and ferments is due to results of inflammation still going on, all spices and unnecessary salt and foods containing them must be forbidden, since they may act as irritants. Although HC 1 is absent, it will be found best not to administer it when it causes symptoms of gastric distress. In these cases, where the mucosa is extremely sensitive and an atrophic gastritis exists, gastric diges- tion had best be converted into an alkaline proteolysis and amylo- lysis by supplying pancreatin. According to recent experiments (Rachford, “Amer. Jour, of Physiol.,” vol. 11) sodium bicarbonate retards pancreatic digestion, and hence its addition to pancreatin is not called for. In these extreme cases of sub- or anacidity it is sometimes found that hydrochloric acid gives pain and even causes emesis. Meats that are given in anacidity must not be too fresh, but properly seasoned and very tender ; they must be thoroughly cooked in a steam broiler until they almost fall apart into the primi- tive muscle-bundles. A practical way is to rub, cut, or scrape the meat prior to cooking it. Finally, if in addition to the anacidity one has reason to believe that duodenal digestion is also disturbed (from chronic duodenitis, occlusion of the pancreatic or bile-duct, or from catarrh, or carcinoma of the duodenum, pancreas, gall- bladder, or liver), then the administration of meat-powders and beef peptones is in order. These substances, which are really albumoses, though capable of satisfying the requirements of metabolism, are not palatable and are relatively expensive. The peptones most frequently used in Germany are those of Kemmerich, Denayer, and Maggi. Ewald and Gumlich (“ Berlin, klin. Wochenschr.,” 1890, No. 44) have investigated the qualities of a “ peptone beer,” and found it quite nutritious. Boas speaks favorably of the American product “ Mosquera ” Julia Beef Meal. Professor R. H. Chittenden (in a report to the Philadelphia County Medical Society, May, 1891) has given the results of his analysis of American beef products, which are found in the following table : 200 DIETETIC TREATMENT OF GASTRIC DISEASES. PERCENTAGE COMPOSITION OF BEEF PRODUCTS, ANALYZED 1891. Constituents. Liebig’s Extract of Beef. Armour’s Ex- tract of Beef. Valentine’s Meat Juice. Wyeth’s Beef Juice. Bovinine. Murdock’s Liquid Food. 1 Johnston’s Fluid Beef. Arlington Chemical Co.’s Beef Peptonoids. Mosquera Beef Meal. Water (at 1 io° C.), 20.06 14.03 60.31 57-88 81.09 83-99 39-58 6.80 6.68 Solid matter (at no 0 C.), . . . 79-94 85-97 39.69 42. 12 18.91 16.01 60.42 93.20 93-32 Soluble in water, . 50.40 48.14 31.26 Insoluble in water, 0 0 0 O 0 0 10.02 45.06 62.06 Inorganic constitu- ents, .... 24.04 28.29 II.30 17-52 1.02 0.66 13-52 5.08 4-23 Phosphoric acid (P 2 0 5 ), .... 9-13 7.28 4.00 3-94 0.03 0.09 3-91 I.40 I.71 Fat, ether extrac- tives, 0.91 I.27 0.78 0.85 1.49 0.27 1.29 2-95 13.60 Soluble in 80 per cent, alcohol, . 55.72 67.92 29.15 35 -o 8 34 -io Total nitrogen, 9-52 8.80 2.68 3-25 2.43 2.29 7.38 4.42 12.36 Nitrogen of insolu- ble matter, . . 1.46 3-25 7-65 Insoluble proteid matter, . . . 9.12 20.30 47.81 Soluble albumin coagulable by heat, . . . . 0.06 0.68 o -55 0.47 13.98 14.29 0 O 0 Soluble albumoses, 0 0 0 0 0 0 0 5-44 11.09 Peptone, ... 0 0 0 0 0 0 0 1.87 18.34 Total proteid mat- ter available as nutriment, . . 0.06 0.68 0-55 0.47 13.98 14.29 9.12 27.61 77.24 Nutritive value as compared with fresh lean beef (lean beef— 100), 0.30 3-50 2.80 2.40 72.40 74.00 47.20 14 30 4CO.00 Armour & Company, of Chicago, manufacture a valuable product which is called “ Vigoral,” containing sixty-eight per cent, albumi- noids. It is a saturated solution, or rather suspension, of pure powdered beef in beef extract. These substances readily decom- pose and should be tested as to their freshness. So the table of Chittenden’s comparisons is valuable only to show the superiority of foods containing the beef in powder or insoluble form, to the extracts, which represent only the soluble salts of the beef and very little of the nitrogenous constituents — rarely more than eight per cent. The Mosquera beef meal is a product that undoubtedly has an exceptionally high nutritive value, the total proteid matter avail- able as nutriment being 77.24 per cent. It also contains 13.60 DIETETICS OF ATONY AND DILATATION. 201 per cent, fat, 1 1.09 per cent, soluble albumoses, and 18.34 per cent, of peptone. With Chittenden’s authority for this analysis, and our own experience as to its easy digestibility and perfect absorption, this product commands an important place in our dietary for sub- or anacidity and gastric atrophy, particularly when associated with intestinal disease. The juice of the pineapple contains a proteo- lytic ferment, thus adapting this fruit for the treatment of cases where no gastric juice is secreted. For its digestive effect only the juice of the fresh fruit should be swallowed, and the fiber removed from the mouth. By boiling the pineapple the proteolytic ferment is destroyed. When atony or pronounced dilatation accompany any gastric disease, particularly those already referred to, the dietetic manage- ment is most important. Weakening and loss of motility are among the most serious affections of the organ, and in the gravity of their consequences outweigh any disturbance of secretion. Motor insufficiency may supervene upon any gastric disease. As a rule, the chronic affections rarely become manifest until the motility is disturbed; that is, until the muscular tonus relaxes. Many times a co-existing secretory or organic disease is the cause of the dilatation ; for instance, it is generally admitted that hyper- acidity can produce spasm of the pyloric sphincter, which the gastric peristalsis will be unable to overcome. In the section on Motor Insufficiency, in the third (clinical) part of this work, the etiology of this affection will be fully considered. When ingesta remain in the stomach longer than normally, fermen- tation, gas-formation, and distention eventually supervene, causing stasis in the muscular layer and dilatation (Naunyn, “ Deutsches Arch. f. klin. Med.,” 1882, Bd. xxxi). In dilatation proper — the deciding sign of which is presence of ingesta in the stomach in the morning after a test-meal taken twelve hours previously — we must, from a dietetic as well as from a therapeutic standpoint, distinguish between the myasthenic, atonic form due to simple relaxation of the muscularis, and the obstructive form due to pyloric or duodenal stenosis. In the first variety dietetic and other treatment may effect a cure. In the stenotic types little beyond transient improvement must be expected, except when the obstacle (cicatrix, carcinoma, hyper- trophied pylorus, gall-stones, peritoneal adhesions, etc.) can be removed permanently or temporarily, or where a new route can be devised for the passage of the chyme. Here abdominal surgery 14 202 DIETETIC TREATMENT OF GASTRIC DISEASES. asserts itself, and gastro-enterostomy has thus far produced the best results. (See chapter on Operative Treatment of Gastric Diseases.) The dietetic management of dilatation will have regard not only to the injured muscular tonus, but also to the secretory or organic disease with which it may be associated. For example, if it is associated with chronic gastritis, the diet must be that for this dis- ease and dilatation ; and if it is combined with hyperacidity, the diet is the one devised for this trouble and dilatation. As the fundamental thing in dilatation is to prevent burdening of the muscularis, the diet must be as light in weight as possible, and espe- cially, as far as practicable, exclude liquids, for these are not only all heavy, but are not at all absorbed from the stomach (excepting alcohol). The requisite amount of water is best given by high sigmoid enemata : y 2 of a liter, slightly warmed, two or three times a day. In this manner a water impoverishment can be prevented (see Wegele, “ Die atonische Magenerweiterung u. ihre Behand- lung”). An absolutely dry diet was suggested by van Swieten, Chomel (“ Les Dyspepsies,” Paris, 1857), and Fossagrives, but its strict execution, as was developed by Schroth, is impracticable, since fully developed dilatations require months, even years, of strict dieting, which, if followed out on these lines, would inevitably produce dangerous drying ,out of the organs (Kussmaul, “ Zur Behandl. d. Magenerweit.,” “ Deutsch. Arch. f. klin. Med.,” Bd. vi). Although it is not a dietetic therapy, yet lavage must be men- tioned here. If large masses of decomposed food are vomited, the stomach-tube is indispensable. Milk diet, used exclusively, aggravates the symptoms without exception. Should the vomit or test-meals reveal that carbohydrates habitually disagree and ferment, an exclusive beef- or meat-diet for a few weeks is rational, and is followed by less distention (Minkowski). In very severe and extreme cases of dilatation one may be com- pelled to feed exclusively by rectal enemata, for the preparation of which we refer to the paragraph on that subject. Soups and drinks during meals must be avoided. Great thirst can be quenched by taking small pieces of ice into the mouth. Patients that are being treated with lavage may be permitted to quench their thirst before the evacuation. Moritz has shown that solid food is retained longer than semisolid ; the latter form is, therefore, preferable. Meats are given best in scraped or finely chopped state, and must be of the red varieties and free from fat. Meat dumplings or balls, DIET IN CARCINOMA. 203 hash of fresh beef or lamb, Mosquera beef-powder, Valentine’s or Wyeth’s juice, or Wiel’s beef-jelly, are adapted to dilatations in which secretion is preserved. When gastric digestion is much lowered the cereal and leguminous products are useful. We recom- mend gruels made from arrowroot, tapioca, rice, sago, cerealin, strained oatmeal, after which we are accustomed to advise some form of diastase, either the taka diastase or malt extract. Aleu- ronat flour, containing much digestible albumin (prepared by Dr. Hundhausen, Hamm, Westphalia, Germany), and the soup meals of C. H. Knorr (Heilbronn, Germany) are of use when prepared according to our dietetic directions. To be digestible, even for healthy stomachs, all leguminous foods must be cooked a long time. For gastric sufferers they must be used only in a condition of very fine subdivision, and partial dextrinization of their starch, rendering it more soluble. Besides the products of this character just mentioned, we have used the Liebig malto-leguminose (pre- pared by William Roth, Jr., in Stuttgart), and the biscuit-legumi- nose (Theodor Fimpe, in Magdeburg). The firm of Hartenstein & Company (Chemnitz, Germany) prepare several good leguminous flours. The Farbenfabriken of Elberfeld, Germany, produce the valuable mixture of albumoses known as somatose , which can be obtained in the form of chocolate, cocoa, and biscuit. Further references in Penzoldt and Stintzing’s “ Handbuch d. Therapie,” vol. iv, pp. 256-258. The collection of dietaries will contain menus for gastric atony and dilatation (1) with loss of secretions or anacidity; (2) with normal or augmented secretions; (3) with serious stenotic symp- toms. In severe cases of the latter type even the most sparing diet by the mouth will be impossible, and as a last resource we must fall back on nutritive rectal enemata. Sometimes after a week to ten days of rectal alimentation, the diseased condition becomes so improved that partial mouth-feeding may be resumed. The diet in the various types of carcinoma coincides with that of motor insufficiency and dilatation whenever the neoplasm is causing the stenosis. In carcinoma of those portions which do not form an obstacle to the exit of the chyme, and where the motility is good, the patient’s appetite must be stimulated as much as possible by strychnin, HC 1 , bitter tonics, condurango, etc., and nothing forbidden, as the physician must be satisfied if the patients eat anything. As chronic gastritis is always present 204 DIETETIC TREATMENT OF GASTRIC DISEASES. even in these cases, the diet list as given for this disease is ad- visable. In cancer arising on the basis of old gastric ulcers, the ulcus carcinomatosum , there is often a pronounced hyperacidity which, naturally, is best met by the diet recommended for augmented gastric secretion, provided the stenosis permits it. Where the stenosis is at the cardia the matter of proper alimen- tation becomes difficult. So long as the stenosis, — no matter from what cause, — can be kept open by bougies and sounds, a highly nourishing liquid diet of milk, eggs, beef-jelly, beef-meal, peptone, nourishing soups con- taining somatose, and wines are indicated. In rare cases we have seen life prolonged by allowing the esophageal tube to remain in situ and feeding through it every two to three hours. Leyden (Leyden-Renvers, “ Deutsche med. Wochenschr.,” 1887, No. 50) and Gersunny (“Wien. med. Wochenschr.,” 1887, No. 43) have strongly indorsed this procedure for esophageal strictures of car- cinomatous origin. After the stenosis is no longer passable, and gastrostomy becomes necessary, in order that nutrition may be carried on through the gastric fistula. According to Friedenwald’s studies on salivary digestion it would be logical to advise these unfortunates to chew their food first, and removing it from the mouth insert it through the fistula. But where this is objected to, it is expedient to add fifteen grains of ptyalin to the food, which must always be liquid or in the form of paste, soup, or gruel. Finally, when gastrostomy can not be done, or permission to per- form it is refused, the only way to nourish the patient is by rectal enemata. So it is evident that the symptoms and dietetic manage- ment of carcinoma vary greatly according to its location. In Sep- tember, 1897, we had under observation a patient who had a gastric tumor, which as far as could be palpated was about four inches long and two inches wide. There has been no evidence of HC 1 secretion for over a year, but, as the motility is very good, there is no lactic acid formation. The Oppler-Boas bacillus has been repeatedly found in the gastric contents when there was temporary food retention. Permission for operation was refused. Still, this patient, with an undoubted carcinoma, gained twelve pounds in six weeks, and had no subjective complaints while in our sani- tarium for digestive diseases. With anacidity and a fair peristalsis a carbohydrate diet is applic- able to carcinoma, but when HC 1 is well tolerated the various DIET IN GASTRIC ULCER. 205 meats must not be forbidden. Of these, Boas prefers the meat from various fishes. Where HC 1 is not well tolerated, pancreatin is in place. Lavage can not be avoided when much fermentation and signs of dilatation are marked; in case these signs are very annoy- ing, a few days of exclusive meat diet or of rectal feeding may be necessary to restore somewhat of the lost gastric tonicity. Long before pyloric stenosis is complete, the case should be transferred to the surgeon, as the resorption from the stomach itself, even if it were normal, is insufficient to maintain life. Those materials that are readily absorbed from a healthy stomach, such as albu- moses, peptone, glucose, and maltose, etc., are given in these cases. There is little evidence, however, of their being absorbed. The good effects of gastro-enterostomy consist not only in the entrance made for the food into the intestine, whereby better digestion becomes possible, but also in an improvement in the inflammatory process around the neoplasm, which is no longer kept in continual irritation by stagnating, fermenting masses of food in constant contact with it. The main reason why operations do not bring as much relief and improvement as is expected is to be sought in the delay in performing them. The Dietetics of Gastric Ulcer and Erosions. — There are three types of gastric ulcer which demand a varying or separate dietetic treatment. These are : (1) Light attacks with pain, hyper- acidity, and pyrosis, but no vomiting of blood. (2) Serious cases that have had hematemesis, and still have signs of it at the time of presentation. (3) Old, chronic, frequently relapsing gastric ulcers. There are forms that run a latent course, void of symptoms until a sudden severe hemorrhage surprises the patient and physician, and possibly terminates the case. Erosions which have no great extension laterally nor toward the depth, and can be recognized by fragments of mucosa found in the wash-water, yield very readily to an exclusive diet of milk combined with rest. During the gastric hemorrhage we advise that nothing at all be given by the mouth, not even water, nor ice pills, — absolutely nothing; but absolute rest, a hypodermic injection of 30^ of ergotol, and, if pain and restlessness are marked, of a gr. of morphin sul- phate hypodermically, and a small ice-bag placed over the epi- gastrium. Wiel claims to have arrested gastric hemorrhage by lavage with cold (io° C.) or hot (42 0 C.) water. Such treatment in profuse bleeding at first impresses one as hazardous. But the author has had very good results from lavage with ice-water in 20 6 DIETETIC TREATMENT OF GASTRIC DISEASES. arresting severe gastric hemorrhage. (See Ewald, “ Philadelphia Med. Jour.,” vol. n, p. 334.) This course has, in a very large number of cases, been, as a rule, very satisfactory. If there is much weakness we use the Boas or Ewald nutritive enemata on the day of and following the hematemesis ; but if the pulse is good we dispense with them. On the day following the hemorrhage, milk in teaspoonful doses is given every half hour; egg-albumen, if it is taken willingly, is more fitting, as it combines with a larger amount of HC 1 , and when diluted it does not stimu- late secretion. Brandy and wine are to some extent irritating to ulcers and excite more secretion ; they are accordingly not given except there be great prostration. On the third day it will be safe to proceed to carrying out a Leube rest cure, with the consecutive order of diet suggested by him or the diet lists proposed by Penzoldt, both of which present four different groups of food-materials. Be- ginning with the simplest and most digestible, they gradually lead up to a more consistent ordinary household menu. Each of these four diet orders must be persisted in from one week to ten days. Penzoldt’s and Leube’s diet orders, together with our explicit diet lists for various stages of gastric ulcer, will be appended. The principle underlying all treatment by food in these cases is to secure the greatest amount of rest and such sub- stances as will combine with the largest amount of HC 1 and relieve the hyperacidity. In a number of cases of ulcer we have found that an amylaceous diet was retained better and caused less pain than scraped beef or soft eggs. It is advised on the same princi- ples as stated on pages 195—19/. In chronic and frequently recurring cases of ulcer, McCall, Anderson (“Brit. Med. Jour.,” May 10, 1890), and H. B. Donkin (“The Lancet,” September 27, 1890), have had excellent results from total exclusion of the stomach from digestion, by feeding with rectal enemata altogether ; some of their cases were nourished in this way for twenty-three days. Riegel (“ Zeitschr. f. prakt. Aerzte,” 1890, No. 2) speaks enthusiastically of this treatment in stubborn cases of ulcer, and Boas reports ten cases, all of which but one were cured by this method, by giving three to four of his nutritive enemata daily for fourteen days. We have a personal experience of twenty-five persistent cases of ulcer treated in this manner, together with nitrate of silver, bismuth subnitrate internally, and rest cure, and are disposed to look upon the treatment with great DIET IN SENSORY NEUROSES. 207 favor. (See Gros, “ Traitement de Malad. de l’estomac par la cure de Repos absolu,” etc.). An ulcer must not be considered cured until there is no more epigastric pain on pressure and the patient gains weight (Gerhardt). The treatment of the sensory gastric neuroses, to be effective, must combine a number of remedial agents with diet. Hyperesthesia , gastrodynia , or gastralgia , and neurasthenia gastric a are morbid states, the treatment of which must be largely directed to the central nervous organs. The same must be said of the motor neuroses : Cardiospasm and pylorospasm, nervous vomiting , rumina- tion , KussmauV s peristaltic unrest , incontinence of the cardia and of the pylorus. These diseases demand electric, hydropathic, climatic, and medicinal measures, with special massage. A very careful investigation into possible causative constitutional morbid states (anemia, gout, rheumatism, tuberculosis, chlorosis, uric acid diathesis) will often reveal a removable underlying etio- logical foundation. Fliess has reported cases of gastralgia and vomiting, emanating reflexly from the nasal mucosa, and has cured them by local treatment (“ Neue Beitr. z. Klinik u. Therapie d. Nasal-Reflexneurose ”). A case of intense gastralgia that came on particularly at night was cured by mercurial inunctions; the author having suspected syphilis, although this was denied by the patient. In a similar way attention to gynecological disorders in the female and genito-urinary diseases in the male have led to the cure of distressing nervous dyspepsias. In the gastric neuroses of motor or sensory type the diet must be based, as in all previous diseases, as far as is expedient, upon the state of the secre- tion and motility. When the general nutrition is disturbed, the plan of treatment most generally adopted is a fattening rest cure according to the principles laid down by Weir Mitchell and Play- fair. This treatment, though not universally applicable, is the one most to be employed in nervous vomiting of hysterical, anemic, and chlorotic origin, and in stubborn cases of anorexia and gas- tralgia. It is somatic and psychical at the same time. We have had ample opportunity to test the dietetic part of this treatment as it has been developed by Burkart in Germany (“ Volkmann’s klin. Vortrage,” No. 245). And cases of the types described have, in our local sanitarium and in the various hospitals with which the author is connected, been completely cured. Of course, organic changes in the digestive organs render the proper nutrition impossible. Contraindications to fattening cures are : Cerebral excitation or 208 DIETETIC TREATMENT OF GASTRIC DISEASES. depression; hysteria, with uncontrollable vomiting; and visceral neuralgias, which are expressions of sympathetic nerve diseases. The best results with Weir Mitchell’s restand fattening cures are obtained in neurasthenic or hysterical anorexia with much emacia- tion, but where there is no organic digestive disease. Wherever the nervous dyspepsia is accompanied by gastritis, atony, or dilatation, fattening cures may easily cause pain, pressure, vomiting, and diar- rhea; so that if such cures are attempted because everything else has been tried, one must be cautious not to persist in systematic introduction of large amounts of food, even in divided portions, as the frequently repeated small portions may accumulate when gastric atony exists, etc., and aggravate the symptoms. Burkart begins with ioo gm. of milk with Zwieback every two hours, and increases it so that two to three liters of milk per day are taken after fourteen days of treatment. The milk may be flavored with sugar, cocoa, tea, lime-water, or salt, according to taste ; and after a few days other articles of diet are cautiously added. We give Burkart’s complete menu among our diet tables. Neurasthenia gastrica (Ewald), or the nervous dyspepsia of Leube, when it occurs in males, is, in our experience, not benefited by the methods of Weir Mitchell or Burkart. Here more than ever the physician must endeavor to remove the cause if possible (excess in tobacco, overwork, uric acid diathesis, sexual overindulgence). A definite diet can not be given, because there are rarely two cases alike ; the dietetic treatment of nervous dyspepsia is difficult, the strictest individualization is requisite. The prognosis as regards perfect recovery is doubtful. An attempt with the Leube or Penzoldt order of dieting is not only rational, but sometimes productive of lasting improvement. The Indications for Predigested Foods: Peptones, Albu- moses, Dextrose, etc. — The idea of supplying foods that would replace the lost digestive function of the stomach or by presenting them in an absorbable form that would spare the work which it had become incapable of performing, was suggested by the recognition of diseases that tended to destroy the glandular apparatus, or caused emesis of the ingested food. In such instances in which the amount of albuminous foods that can be taken is very small, the question has been raised whether peptones are able to equalize the deficit of albumin requirement. As a certain amount of albuminous food is indispensable to life, whenever the quantity ingested sinks below the so-called thresh- USE OF PREDIGESTED FOODS. 209 old value of albumin (“ Schwellenwerth ”), health begins rapidly to decline. Deiters has shown (von Noorden, “ Beitr. z. Lehre v. Stoffverlust d.gesund. u. krank. Menschen,” Heft 1, 1892) that even when the amount of albumin ingested sinks below the threshold value, peptones and albumoses (Denayer’s mixture) are capable of maintaining the body in nitrogenous equilibrium. Kuhn confirmed this observation in Riegel’s laboratory with regard to an albumose mixture selling under the name of somatose ; so that we may con- clude that these products can replace food-albumin for a time at least ; still, we doubt very much whether it is expedient or neces- sary to give peptones and albumoses in larger quantities. Their expensiveness would be no serious objection if the advantages of their use were very obvious. In secretory insufficiency of the stomach it is well known that the proteolytic power of the intestine will utilize most of the unal- tered proteid. Even where the stomach is excluded from digestion entirely, albumin is used up to a sufficient degree (Ogata, “ Arch. f. Anat. u. Physiol.,” 1883, S. 89). Loss of peptic function, therefore, does not prevent sufficient utilization of albumin. There is an apparent advantage in the bland and unirritating quality of albumoses, but certainly this is possessed also by certain undigested foods (milk, egg-white). Peptones and albumoses are not absorbed more readily when ingested ready-formed, than when they are first devel- oped from albumin in the stomach (Cahn, “ Die Verwendung d. Pepton als Nahrungsmittel,” “ Berlin, klin. Wochenschr.,” 1893, No. 24). They are said to produce diarrhea; but to establish this fact, the quantity of artificial peptone and the amount of nitrogen in the remaining ingesta must be considered together, for the diarrhea may be due to excess of nitrogenous food, which may be given unknowingly, since it is impossible to determine the total nitrogen ingested, except by quantitative analysis. As an indication for the use of predigested foods, we may state the conditions where the albumin-dissolving power of the stomach is permanently reduced or lost, where the amount of meat- and egg-ingestion becomes insufficient because of efforts necessary to avoid mechanical irritation. If duodenal digestion is also deranged, the indication becomes more urgent. When the secretory func- tion is lost, but the motility preserved, the vicarious intestinal pro- teolysis will digest sufficient proteid. When peristalsis is, how- 210 DIETETIC TREATMENT OF GASTRIC DISEASES. ever, also lost, then the administration of peptones is of no benefit, for we agree with Cahn (loc. cit.) that in gastrectasia dependent upon pyloric stenosis, peptones are not absorbed, but remain in the stomach just as water does. Riegel (loc. cit., p. 241), considers this deduction of Cahn’s as erroneous, because von Mehring has shown that the stomach does absorb peptone. To this we would reply, that von Mehring did not experiment upon dilatations de- pendent upon stenosis, but upon normal stomachs. In his experiments Cahn found that peptone causes an increased flow of the gastric juice, and suggested that therefore it should not be given in hyperacidity and hypersecretion, in which evi- dently it is quite unnecessary, as in these secretory abnormalities meat and egg are digested excellently. In ulcer, albumoses may find temporary usefulness because of their unirritating qualities, which, of course, would be counterbalanced by their effect in increasing the HC 1 , should Cahn’s conclusion prove true. Pure peptone represents a proteid not coagulable by boiling nitric acid, acetic acid, ferrocyanide of potash, nor ammonium sulphate. Such a peptone has, in our experience, no field of usefulness in practical dietetics. It is an irritant to the mucosa of the digestive canal and has an intolerably bitter taste. In conclusion, we may state our personal custom in the use of these substances. Whenever the ingestion of albumin in the food becomes insufficient, or even where it is ingested in sufficient amounts for a healthy individual, but owing to some consuming disease, such as carcinoma (not hindering peristalsis), tuberculosis, etc., it can not cover the nitrogen equilibrium, in the amounts possible to eat in ordinary diet, then we employ albumoses liber- ally, and generally so mixed with the food (soups, scraped broiled meats, in puree) that the patient can not detect them ; for this pur- pose the tasteless and odorless products — somatose, Mosquera beef-meal, etc. — are preferable. Rectal Alimentation. — In diseases in which the approach to the stomach is stenosed (carcinoma or stenosis of the esophagus or cardia), or in which the organ requires a temporary but absolute exemption from work (ulcer and some forms of gastritis), or in cases in which the mildest and most digestible diet is not tolerated, it becomes necessary to support the strength by nutritive rectal enemata. The history of the evolution of the nutritive enema is, from a physiological standpoint, very interesting ; and as the author has RECTAL ALIMENTATION. 2 I I at various times done considerable experimental work in this line, a brief review of the same is believed essential to a proper under- standing of the subject. The first to discover that the human colon and rectum absorbed an emulsion of eggs and water only when sodium chlorid was added were Voit and Bauer (“ Zeitschr. f. Biol.,” 1869, Bd. v). They found that these foods were not absorbed in the absence of salt, and in 1871 Eichhorst (“ Phliiger’s Archiv,” Jahrgang iv, 71) con- firmed their results. Injections of bouillon, milk, and eggs had been used long before this time, but no one ever attempted to ascertain to what degree the mucosa of the large intestine would absorb it. In 1872 Leube proposed a meat-pancreas injection (“ Deutsch. Archiv f. klin. Med.,” Bd. x, Reihe in), the plan emanat- ing from the idea to transpose something of the character of pancre- atic digestion into the large intestine. The preparation of this useful enema is as follows: Take 150 to 300 gm. of very finely scraped beef and 50 to 100 gm. of finely chopped pancreas of the calf or pig, and mix with the addition of 150 c.c. luke-warm water in a bowl ; if desired, 25 to 50 gm. of fat may be added in the form of oil or butter; the injection must be made at the body-temperature. We have convinced ourselves that this mixture digests thor- oughly in the large intestine ; its preparation is complicated, how- ever, requiring very intimate mixing, and it rapidly decomposes. Leube reported a case which he kept alive six months by this enema exclusively, and in a similar way Riegel nourished a case of esophageal stricture for ten months. Ewald demonstrated that egg-emulsion is absorbed without being peptonized or salted (“ Zeitschr. f. klin. Med.,” Bd. 11), and Huber, while confirming Ewald’s observation, added that the addition of salt, or pre- vious peptonizing, really doubled the amount of emulsified eggs that was absorbed in the colon. Eggs, it must not be over- looked, contain a considerable amount of normal salt, and this may explain Huber’s results (“ Zeitschr. f. klin. Med.,” Bd. xlvii) as to their absorption in part, even without the addition of salt. But it is an established fact that the addition of sodium chlorid very much increases the amount of eggs that is absorbed. In a very interesting series of experiments Grutzner offered a physiological explanation of this phenomenon (“ Deutsche med. Wochenschr.,” 1894, No. 48), having demonstrated that under cer- tain conditions particles of charcoal, finely cut horse-hair, or saw- dust, impregnated with normal (0.6 per cent.) salt solution and 212 DIETETIC TREATMENT OF GASTRIC DISEASES. injected into the rectum of rabbits, guinea-pigs, and rats, are found six hours later all along the small intestine, even in the stomach, while the rectum is empty. During a period of twenty-four hours before these injections the animals were starved. When the suspensions of these particles were made in distilled water, HC 1 solution, or potassium chlorid solution, instead of physiological salt solution, the particles did not ascend in the digestive tract. Griitzner injected starch-suspensions in normal NaCl solution into the rectum of human beings, and after a number of hours demon- strated starch-grains in the gastric contents, microscopically. Nothnagel first showed that sodium chlorid placed on the serous surface of the intestine is capable of starting antiperistaltic move- ments (“ Beitrag z. Physiol, u. Pathol, d. Darms,” 1884), and Griitzner interprets this observation as an explanation of the digestion of egg-enemata containing salt. He assumes that the injected mass is moved upward through the entire small intestine, and so becomes digested and absorbed. Even Riegel ( loc . cit., p. 245) is satisfied with this interpretation, and adds that it ex- plains the negative results of Voit and Bauer without salt, and the positive ones with salt, and also those of Huber. In our opinion, the evidences that food-substances move anti- peristaltically upward in the intestine are not satisfactorily given in Grutzner’s work. It is undeniable that minute particles of starch, charcoal, etc., are moved from the rectum toward the stomach in man ; and we have been able to confirm this part of his results, as well as the fact that salt favors the ascent and HC 1 and KC 1 im- pede it. But this antiperistaltic motion we conceive to be only a very feeble marginal ascending movement, effected by surface con- tact of the particles with the epithelium, which in turn is moved by the muscularis mucosae. This very slight marginal antiperistalsis is never visible to the eye, and can only be demonstrated by the progress of particles ; it is not capable of propelling food masses ; on the contrary, we have convinced ourselves that at the same time that the marginal peristalsis drags visible particles of charcoal toward the stomach with infinitesimal slowness, there may be an uninterrupted current of central food masses toward the anus. The marginal antiperistalsis may be a physiological thing, present at all times, and its object may be the raising or drawing up of portions of mucosa from one place to another in order to bring new surfaces in contact with the ingesta, or to replace a portion of surface to its normal topography after it has been dragged away from it by the PATHOLOGICAL ANTI PERISTALSIS. 213 downward current. The cohesion of these small particles with the mucosa can be seen when a piece of fresh animal intestine is sprinkled with lycopodium or finely cut horse-hair particles and held under a gentle stream of water; the gut may be moved upward on the surface of the hand while the water moves down- ward, and still many of the particles will adhere. The antiperistalsis that Nothnagel produced by placing crystals of salt upon the serosa is quite a different thing, for it is plainly visible to the eye, and never occurs under physiological conditions (Nothnagel, “ Erkrank. d. Darms,” portion on “ Die Darmbewe- gung,” p. 6, 1896). Among the abnormal conditions that may cause this visible antiperistalsis, Nothnagel states stronger solu- tions of sodium chloridand the introduction of food at an unphysio- logical entry, as which in man we must consider the rectum. He adds ( loc . cit.) that from a physiological entry,/. ^.,from the stomach, the strongest chemical irritants produce only peristaltic movements toward the anus. There are, then, two kinds of antiperistaltic move- ments: (1) Those of Griitzner, being marginal, invisible, possibly physiological, and not capable of moving food masses ; (2) those of Nothnagel, being visible, strong, and occurring only under abnormal conditions. Christomanos, a pupil of Nothnagel, has urged an objection against Grutzner’s results that seems to invali- date the conclusions of the latter ; namely, he found (Christomanos, “ Z. Frage d. Antiperistaltik,” “ Wien. klin. Rundschau,” 1895, Nos. 12 and 13) that when his animals were prevented from licking up the expelled rectal contents his results as to finding the particles in the stomach were negative. Dauber came to the same conclusion as Christomanos, namely, that the occurrence of particles of rectal injections in the stomachs of animals did not take place when they were prevented from eating their excrement. These objections are, however, set aside by Grutzner’s and our own observations on the human subject. The experiments of Swiezynski (“ Deutsche med. Wochenschr.,” 1895, No. 32) also confirmed Grutzner’s statements, in that lycopodium injected into the rectum was found in the stomach. We must, however, again emphasize that this antiperistalsis is not capable of moving ingesta, and that it can not logically be taken as an explanation of the digestion of enemata. The fact that normal salt solution favors the invisible marginal ascent of particles, and that other chemicals impede it, is perfectly natural. For if this antiperistalsis be physiological, and be assumed 214 DIETETIC TREATMENT OF GASTRIC DISEASES. to be going on at all times, normal salt solutions can not disturb it, for they are the physiological environment in which all intestinal movements occur. But HC 1 and KC 1 are chemical irritants, to which the muscularis mucosae reacts by efforts at expulsion. The Occurrence of Proteolytic Ferments in the Colon and Rectal Contents. — The author’s explanation of the digestion of egg and milk emulsions in the rectum and colon is quite different from Griitzner’s and from that accepted by Riegel and others, and is based on a very carefully conducted series of experiments on animals and human beings. We desire to speak only of actual digestion, for there is good reason for believing that albumin, fats, etc., may be absorbed from the large intestine as such — without digestion. Without going into the details and technic of these experiments, we will briefly state the conclusions. After the rectal contents of dogs or cats are sterilized with saturated solutions of thymol (so strong that the crystals float on top) and passed through a Pasteur filter, control cultures are made to ascertain that the watery extract of the excrement is sterile. For this purpose the meat pepton- gelatin and agar plates recommended by Nothnagel ( loc . cit ., p. 22) are most convenient. The reaction of human excrement is gener- ally weakly alkaline or neutral; very rarely weakly acid under normal conditions. This watery extract of normal rectal contents contains a substance which in a digestorium (thermostat at 40° C.), and in an alkaline medium (equal to from 0.8 to 1 per cent. Na 2 C 0 3 ), dissolves from 36.3 to 30 - per cent, of Merck s' dried serum-albumin in three hours under aseptic conditions. It will also digest fibrin, and has, in addition, a faint amylolytic power, converting from 10 to 14.5 per cent, of starch into maltose in an alkaline medium of 0.3 per cent. Na 2 C 0 3 . We have not been able to find any fat- splitting action in this extract. As there are many bacteria that produce peptone in the break- ing down of proteid, and others that ferment carbohydrates, the previous sterilization is necessary in order to exclude their action. Bacteria do not make peptone for any philanthropic pur- poses ; the peptone they give rise to is an intermediate stage in a long series of decomposition products. It does not remain peptone, but is rapidly decomposed into amido-acids, ammonia, tyrosin, etc., and does not occur in the intestine as peptone pure and simple, but mixed with a number of other derivatives of albumen, some of which are proven to be toxic. We state this because even among RECTAL CONTENTS AFTER STERILIZATION. 21 5 medical men the opinion has been encountered that the bacterial peptone might be of utility to the organism in which it is formed. The feces for our purposes can not be sterilized by heat, because that Would destroy any possible enzymes present. It is certain, therefore, that rectal contents contain a proteolytic ferment ; also one having a slight amylolytic power, acting only in a faintly alkaline medium, the action being destroyed in an acid medium. Whether these two digestive actions are carried out by one and the same ferment or by two different ferments we are unable to say. That it can not be pepsin is proven by the fact that it does not act in an acid, but only in an alkaline, medium. It would be interesting to learn whether the walls of the large intestine secrete any proteolytic ferment. The colon of a dog that is kept clear of fecal masses by making an abdominal fistula and sewing it to the abdominal wall at the ileocecal valve, secretes an alkaline fluid, which has no proteolytic powers whatever, but there is an evident amylolytic ferment contained in it. The human colon can be plugged up in the transverse portion by introducing a balloon and blowing it up ; thereafter the part be- tween the rubber balloon and the anus is washed out with sterile normal salt solution. A secretion is formed in two to three hours, and can be collected on absorbent cotton placed in the rectum, and later squeezed out into a small beaker. The secretion is alka- line, but has, after filtration through a Pasteur filter, no proteolytic power. Therefore, it is reasonable to assume that the ferment we have demonstrated is derived from the pancreas. In two patients with total atrophy of the gastric mucosa (atrophic gastritis), as evidenced by fragments of the mucosa found in the wash-water, the same proteolytic ferment was demonstrable in the colon contents. It was hitherto assumed that the ferments of the pancreas were destroyed in the intestine (see Rosenheim, “ Die Erkrank. d. Darms,” p. 46). A large number of similar experiments as above described justifies the belief, however, that trypsin and perhaps amylopsin may survive the passage through the bowel. Busch has shown that digestion may go on in the human intestine with- out gastric or pancreatic juice, without bile and secretion of Brunner’s glands (Brficke’s “ Vorlesungen fiber Physiologie,” Wien, 1885, p. 352). The patient on whom Busch experimented had received an abdominal injury by an accident, in such a manner that the gastric juice, together with the chyme, pancreatic juice, duodenal secretions, and bile, ran outward through a fistula. 2 l6 DIETETIC TREATMENT OF GASTRIC DISEASES. Thereafter, Busch fed him through the fistulous opening communi- cating with the lower bowel, and succeeded in maintaining the nitrogenous equilibrium. He lowered coagulated albumin inclosed in small cotton bags into the bowel, and drew them out by a string five hours later, finding that from five to thirty-five per cent, of the albumin was dissolved. In Busch’s experiments the action of the bacteria can not be excluded. The action of the succus entericus may explain the carbohydrate digestion, but, as no proteolytic ferment could enter the small intestine, the digestion of albumin was probably due to bacteria. In conclusion we may say that rectal enemata are digested probably by pancreatic ferments passing through the bowel, by bacteria, and by the succus entericus, which, even in the colon, has an amylolytic action ; that certain foods — egg-albumen, fats, milk — can be absorbed as such without being digested. Griitzner’s marginal ascending motion of particles can not move ingesta upward. F. Mall (“Johns Hopkins Hospital Reports,” vol. i, p. 70) holds that the propelling force of the intestines normally acts in one direction only ; the antiperistalsis is found only as a pathological phenomenon, and all of his efforts to force the intestine to work in the wrong direction by reversal (loc. cit ., p. 93) were negative. Under conditions of great irritation rectal contents may be vomited. Preparation of Rectal Enemata : Indications and Methods of Administration . — The preparation of Ewald’s, Leube’s, and Boas’ nutritive enemata is given under the dietetic tables. Jaccoud recommends 250 gm. of bouillon, 120 gm. of wine, yolks of two eggs, 5 to 20 gm. of peptone. Rosenheim uses peptone (one to two drams), two eggs, 15 gm. of glucose, and some- times, if desired, emulsions of cod-liver oil. Singer’s enema (“ Cen- tralblatt d. ges. Therap.,” Marz, 1895) is very much like that ot Boas, with the addition of peptone. These examples will amply suffice for all purposes. Method and technics of rectal feeding : (1) Every nutritive injection must be preceded by a cleansing in- jection one hour previously. (2) The amount of injected nutriment must not exceed of a liter (Sviij) at a time. (3) After the injection the patient must remain in the recumbent position for one hour, and a hot towel should be held firmly against the anus for fifteen or twenty minutes. PREPARATION OF NUTRITIVE ENEMATA. 2 1 / (4) The patient should lie on his left side with his hips raised upon a pillow, and the injection must be given very gradually. (5) If the rectum is very irritable, the addition of a few drops (10 to 20) of tincture of opium is serviceable. (6) The injection should be made with a funnel or an irrigating bottle, never with a syringe. The best tube to use is that named after Langdon, as it is sufficiently soft and flexible and can not kink upon itself. (7) The tube should, in adults, be passed high up into the colon ; if possible, 14 to 18 inches should be introduced, but 12 inches will, as a rule, suffice. The higher up the enema is placed, the less will be the liability of its rejection. An anatomical and physiological reason for placing injections high is found in the nature of the anastomoses of the vascular supply of the rectum, sigmoid, and colon. The superior rectal and sigmoid veins communicate with the inferior mesenteric vein, therefore these veins conduct whatever they have absorbed directly to the liver through branches of the vena porta. In the liver the very important secondary digestion takes place. The veins from the lower third of the rectum com- municate with the inferior vena cava, and their contents are not conducted to the liver. (8) The temperature of the injection should be that of the body —98.6° F. Indications Necessitating Rectal Feeding. — There are two classes of conditions in which nutritive enemata are indicated : I. The first class comprises patients that are still able to swallow food and willing to do so, but on account of the existence of some gastric, esophageal, or duodenal disease it is necessary or expedient to rest the stomach and exe'mpt it from work. These are : (1) Gastric Ulcer. — For the purpose of keeping the ulcer free from irritation and permitting it to heal or to prevent the starting up of hematemesis. (2) Dilatations. — Either in the atonic or benign forms, to attempt a cure by relieving the stomach of the weight of ingesta and the constant fermentation; or in the malignant, pyloric, and stenotic forms, because food positively can not pass the pylorus and gastro- enterostomy is refused or impossible. (3) Severe gastric irritations, as in toxic gastritis. (4) Exhausting diseases, especially the infectious types, where secretion and absorption are 'inhibited and food not retained, though swallowed. 15 2 I 8 DIETETIC TREATMENT OF GASTRIC DISEASES. (5) Ulcer of the esophagus or duodenum, stricture, ileus, invag- ination, volvulus, stenosis of any part of the alimentary tract be- tween stomach and rectum. II. The conditions in which the patients are unable to swallow food are : (1) Temporary obstruction to the entrance of food into the ali- mentary canal ; presence of new growths ; foreign bodies ; acute inflammations about mouth, pharynx, and esophagus. (2) Extreme sensitiveness of the mouth and esophagus excited by corrosive poisons. (3) Carcinoma, cicatricial contraction, diverticulum, neoplasms, of esophagus ; carcinoma of cardia. (4) Reflex vomiting, as in pregnancy and sea-sickness. There are other states in which the patients are either unable or unwilling to swallow food, but in these feeding by the tube is prefer- able to rectal feeding. These are : ( a ) Inability to swallow from coma, delirium, or paralysis of the muscles of deglutition ; post- diphtheritic paralysis. ( b ) Insanity, refusal of food. ( c ) Total anorexia (hysterical, etc.). Intravascular and Hypodermic Feeding . — In 1850 Hodder first practised intravenous injection of milk in cases of collapse from chol- era Asiatica. T. G. Thomas about this time published a case in which y 2 of a pint of milk warmed to body-temperature was injected into one of the brachial veins, with the result of saving life. According to Gilman Thompson {loc. cit., ,p. 383), Fowler has practised intravenous injection of peptone and has also given six ounces of digested beef solution in this manner. There seems to us no physiological reason why intravenous or even intra-arterial feeding should not be practised in emergencies. As a safeguard, however, we would suggest that every precaution be taken to have the injection absolutely sterile, and composed of such substances as are normal to the blood, such as serum-albumin, sterile plasma, defibrinated fresh sterile blood. Much careful experimenting is required, however, before we can be justified in using such methods on the sick human being. Intravenous and intra-arterial injections of warm, sterile, normal salt solutions have been ex- tensively used in Asiatic cholera and in exhausting hemorrhages. We have had occasion to use them in hematemesis after gastric ulcer, with the conviction that life was saved thereby. Transfu- sion of sterile, normal salt solution into the areolar connective tissue of the breast is to be preferred to these methods, because it SUBCUTANEOUS FEEDING. 2\CJ requires only a pressure-bottle and sterile, sharp-pointed cannula — no other instruments. Subcutaneous Feeding . — In 1869 Menzel and Perco injected fats, albumin, and sugar into dogs and human beings, and showed that liquid oils were resorbed without causing local or general reaction. They injected nine gm. of oil into one patient, at Billroth’s clinic, who had spinal caries; a swelling as large as a silver dollar ensued, but disappeared entirely in thirty hours (“ Wiener med. Woch- enschr.,” 1869, No. 31). Attempts have been made in the human being with injection of defibrinated calf’s-blood by Landenberger (“ Wurtemberg. med. Correspondenzbl.,” Bd. xliv , No. 20), with olive oil by Krueg (Re- ferat in “ Wien. med. Wochenschr.,” 1875, No. 34), with olive oil and milk by Whittaker (“ Schmidt’s Jahrb.,” Bd. clxxvii , Heft 1), who in eight sittings injected 124 gm. in one day — in all he made 68 injections. Karst recommended defibrinated blood (“ Berlin, klin. Wochenschr.,” 1873, No. 49). Eichhorn was so enthusiastic with his injections of milk-peptone and cod-liver oil that he be- lieved the normal nutrition of an animal could be supplanted by this method (“Wien. med. Wochenschr.,” 1881, Nos. 32, 33, and 34). Leube proved that oils injected subcutaneously were actu- ally used up in the metabolism of the body (Leube, “ Verhand- lung. d. XIV. Congresses f. innere Medicin,” 1895). In a case of benign hyperplastic pyloric stenosis complicated by colitis, the author and his associate, Dr. Harry Adler, injected 24 gm. of sterilized olive oil under the skin daily for three weeks. Nutritive enemata were not tolerated on account of the colitis. The oil injections which did not cause the slightest irritation, were absorbed in from four to twelve hours, and, though no analyses on meta- bolism could be executed, it became evident that the patient was benefited by the hypodermic use of oil. In spite of these experi- ments, it is very doubtful whether subcutaneous injections of nutri- tive materials can ever be utilized to supplant normal feeding. The caloric value of the amounts that are available for injection is comparatively insignificant, the method quite irritating, and in progressed sufferers hardly justifiable. 220 APPROXIMATE ANALYSES OF A MAN. TABLES OF DIETETICS. APPROXIMATE ANALYSES OF A MAN. — (Moss.) (Height, 5 feet 8 inches ; weight, 148 pounds.) Pounds. Oxygen 92.4 Hydrogen, .... 14.6 Carbon, . 31.6 Nitrogen, 4.6 Phosphorus, 1.4 Calcium, 2.8 Sulphur, 0.24 Chlorin, 0.12 Sodium, . . Iron, . . . . Potassium, . Magnesium, . Silica, . . . Fluorin, . . Total, Pounds. 0.12 0.02 0-34 0.04 ? 0.02 148.30 Landois and Stirling 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. O. 120 gm. of albumin, containing, .... 90 gm. of fats, containing, 330 gm. of starches, containing, .... 64.18 70. 20 146.82 8.60 IO. 26 20.33 o° bo . . 00 28.34 9-54 162.85 281.20 39-19 18.88 200.73 Add 744.11 gm. of O from the air by respiration. “ 2,818.00 “ of H 2 0. “ 32.00 “ of inorganic compounds (salts). The whole is equal to three kilogm. and a half (seven pounds), i. e., about one-twentieth of the body-weight ; so that about six per cent, of the water, about six per cent, of the fat, about one per cent, of the albumin, and about 0.4 per cent, of the salts of the body are daily transformed within the organism. An adult doing a moderate amount of work gives off in gm. : Water. C. H. N. O. By respiration, 330 248.8 ? 651-15 By perspiration, 660 2.6 7.2 By urine, . . . 1,700 9.8 3-3 15-8 11. 1 By feces, 128 20.0 3-o 3-o 12.0 2,818 281.2 6-3 18.8 681.45 STANDARDS FOR DAILY DIETARIES. 22 I STANDARDS FOR DAILY DIETARIES . — [Compiled by Atwater.) Weights of nutrients and calories of energy (heat-units) in nutri- ents required in food per day : Nutrients. Potential Protein. Fats. Carbo- hydrates. Total. Energy. Gm. Gm. Gm. Gm. Calories. Children to a year and a half, . 28 (20-36) 37 (30-45) 75 (60-90) 140 767 Children of two to six years, . 55 (36-70) 40 (35-48) 40 (100-250) 295 1,418 Children of six to fifteen years, 75 (70-80) 43 (37-50) 325 (250-400) 443 2,041 Aged women, 80 50 260 390 1,859 Aged men, 100 68 35o 518 2,477 Woman at moderate work, Voit , 9 2 44 400 536 2,426 Man at moderate work, Voit f . 118 56 500 674 3 >°5 5 Man at hard work, Voit , . . . Man at moderate exercise, Play- H5 100 45° 695 3,370 fair, Active labor, Playfair , . . . 119 5i 53i 701 3, *39 156 7i 568 795 3, 6 29 Hard labor, Playfair , .... Woman with light exercise, At- 185 7i 568 824 3,748 water, Man with light exercise, At- 80 80 300 460 2,300 water , 100 1 00 360 460 2,820 Man at moderate work, Atwater, 125 125 45° 700 3,520 Man at hard work, Atwater , . Man at moderate work, Mole- 150 150 500 800 4,060 schott, 130 40 55o 720 3,160 Man at moderate work, Wolff, 120 35 540 695 3,032 Table of analyses made by Dujardin-Beaumetz, showing the pro- portion of nitrogen present and also the combustibles calculated as carbon : Nitrogen. C + H Combustibles Calculated as Carbon. Beef, uncooked, 3.00 II. OO Roast beef, . . 3-53 17.76 Calf’s-liver, 3-09 15.68 Foie gras, 2. 12 65-58 Sheeps’ kidneys, 2.66 12.13 Skate, 3.83 12.25 Cod, salted, 5.02 16.00 Herring, salted, 3-ii 23.00 Herring, fresh, 183 21.00 Whiting, 2.41 9.00 Mackerel, 3-74 I9.26 222 STANDARDS FOR DAILY DIETARIES. Table of analyses showing the proportion of nitrogen and combustibles calculated as carbon ( Continued ). Nitrogen. C + H Combustibles Calculated as Carbon. Sole, 1.91 12.25 Salmon, 2.09 16.00 Carp, 3-49 I2.IO Oysters, 2.13 7.18 Lobster, uncooked, 2-93 10.96 Eggs, 1.90 13-50 Milk, cow’s, 0.66 8.00 Cheese (Brie), 2-93 35-oo Cheese (Gruyere), 5.00 38.00 Cheese (Roquefort), 4.21 44-44 Chocolate, 1-52 58.00 Wheat (hard southern, variable average), 3.0° 41.00 Wheat (soft southern, variable average), 1. 81 39.00 Flour, white (Paris), . . . 1.64 38.50 Rye flour, i-75 41.00 Winter barley, 1.90 40.00 Maize, 1.70 44.00 Buckwheat, - 2.20 42.50 Rice, 1.80 41.00 Oatmeal, i-95 44.00 Bread, white (Paris, 30 per cent, water), 1.08 29.50 Bread, brown (soldiers’ rations formerly), 1.07 28.00 Bread, browm (soldiers’ rations at present), 1.20 30.00 Bread from flour of hard wheat, 2.20 3 I -oo Potatoes, °-33 11. 00 Beans, ... 4-5° 42.00 Haricots, dry, 3-92 43.00 Lentils, dry, 3-87 43-oo Peas, dry, 3- 66 44.00 Carrots, 0.31 5-50 Mushrooms, 0.60 4-52 Figs, fresh, 0.41 15.50 Figs, dry, 0.92 34-co Plums, 0-75 28.00 Coffee (infusion of 100 gm.), 1. 10 9.00 Tea (infusion of 100 gm ), 1. 00 10.50 Bacon, 1.29 71.14 Butter, fresh, 0.64 83.00 Olive oil, 98.00 Beer, strong, 0.05 4-50 Wine, 0.15 4.00 THE RELATIVE VALUE OF FOODS. 223 TIIE RELATIVE VALUE OF FOODS. — ( Scam null. ) (The figures represent percentages.) Articles. As Mate- rial for THE Muscles. As Heat Givers. As Food FOR THE Brain and Nervous System. Water. Waste. Wheat, 14.6 66.4 1.6 14.0 3-4 Barley, 12.8 52.1 4.2 14.0 16.9 Oats, 17.0 50.8 3-0 13.6 16.9 Northern corn, 12.3 67-5 1. 1 14.0 51 Southern corn 34-6 39-2 4.1 14.0 8.1 Buckwheat, 8.6 53 -o 1.8 14.2 22.4 Rye, 6.5 75-2 o -5 13-5 4-3 Beans, 24.0 40.0 3-5 14.8 17.7 Peas, 23-4 41.0 25 14. 1 19.0 Lentils, 26.0 39 -o i -5 14.0 19.5 Rice, 5-1 82.0 o -5 9.0 3-4 Potatoes, 1.4 15.8 0.9 74.8 7-1 Sweet Potatoes, i -5 21.8 2.9 67.5 6.3 Parsnips, 2.1 14-5 1.0 79-4 3 -o Turnips, 1.2 4.0 o -5 9 °. 4 3-9 Carrots, 1. 1 12.2 1.0 82.5 3-2 Cabbage, 1.2 6.2 0.8 9 i -3 o -5 Cauliflower, 3 - 6 4.6 1.0 90.0 0.8 Cucumbers, 0. 1 i -7 0.5 97.1 0.6 Milk of cow, 5 -° 8.0 1.0 86.0 Milk, human, 3 -o 7.0 o -5 89-5 Veal, 17.7 14.3 2-3 65-7 Beef, 19.0 14.0 2.0 65.0 Lamb, 19.6 14-3 2.2 63-9 Mutton, 21.0 14.0 2.0 63.0 Pork, 17-5 16.0 2.2 64.3 Chicken, 21.6 1.9 2.8 73-7 Codfish, 16.5 1.0 2-5 80.0 Trout, 16.9 0.8 4.3 78.0 Smelt, 17.0 very little 5 or 6 75 -o Salmon, 20.0 some fat 6 or 7 74.0 Eels, 17.0 “ 3 or 4 75 -o Herring, 18.0 “ 4 or 5 75 -o Halibut, 18.0 “ 3 or 4 74.0 Oysters, 12.6 0.2 87.2 Clam, 12.0 very little 2 or 3 Lobster, 14.0 “ 5 or 6 79-9 Eggs, white of, 13.0 2.8 84.2 Eggs, yolk of, 29.8 2.0 51-3 Butter, 100. 0 Artichoke, i -9 19.0 ’ 1.8 76.6 0.7 Asparagus, 0.6 5-4 0.4 93-6 Bacon, 8.4 62.5 o -5 28.6 Carp, 18.0 0.8 2.9 78.3 Cheese, 30.8 28.0 4-7 3 6 -5 Cherries, 0.6 21.0 1.0 76.3 1. 1 Chocolate, 8.8 88.0 1.8 1 4 Cream, 3.5 4-5 92.0 Currants, 0.9 6.8 °-3 81.3 10.7 Dates, fresh, 73-7 24.0 2.3 Figs, 5 -o 57-9 3-4 18.7 i 5 -o Ham, 35 -o 32.0 4.4 28.6 Horse-radish 0. 1 4-8 1.0 78.2 16.0 224 PERCENTAGES OF NUTRITION, ETC, THE RELATIVE VALUE OF FOODS ( Continued ). Articles. As Mate- rial for THE Muscles. As Heat Givers. As Food for the ' Brain and Nervous System. Water. Waste. Kidney, 21.2 0.9 1.4 76.5 Lard, loo. 0 Liver, 26.3 3-9 1.2 68.6' Onions, 0-5 5-2 o -5 93-8 Pearl barley, 4-7 78.0 0.2 9-5 7.6 Pears, 0. 1 9.6 864 3-9 Pigeon, 23.0 1.9 2.7 72.4 Prunes, 3-9 78.6 4-5 13.0 Radishes, 1.2 7-4 1.0 89.1 i-3 Suet, 100.0 Venison, 20.4 8.0 ' 2.8 68.8’ Vermicelli, 47-5 38.0 i-7 12.8 Whey, 4.6 0.7 94-7 ATKINSON’S TABLE OF DIGESTIBILITY OF NUTRIENTS OF FOOD MATERIALS. In the Food Materials Below. Of the Total Amounts of Protein, Fats, and Carbo- hydrates, the Following Percentages were Digested : Protein. Fats. Carbohydrates. Meat and fish, Practically all 79 to 92 Eggs, “ 96 Milk, 88 to 100 93 to 98 ? Butter, 98 . . . Oleomargarine, 96 Wheat bread, 81 to 100 ? 99 Corn (maize) meal, 89 ? 97 Rice, 84 ? 99 Peas, 86 ? 96 Potatoes, 74 ? 92 Beets, 72 ? 82 PERCENTAGES OF NUTRITION IN VARIOUS ARTICLES OF FOOD.— Raw cucumbers, Raw melons, Boiled turnips, Milk, Cabbage, Currants, Whipped eggs, Beets, Apples, Peaches, Boiled codfish, Broiled venison, Potatoes, . . . Fried veal, 24 Roast poultry, 26 Raw beef, 26 Raw grapes, 27 Raw prunes, 29 Boiled mutton, 30 Oatmeal porridge, . 75 Rye bread, 79 Boiled beans, 87 Boiled rice, S8 Barley bread, 88 Wheat bread, 90 Baked corn bread, 91 Boiled barley, 92 Butter, 93 Boiled peas, 93 Raw oil, 96 ( Moss. ) ■ 3 \ x /z ■ 7 • V/z 10 13 , 14 , 16 REQUISITE FOOD PERCENTAGES IN HEALTH. 225 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 Cent. Water, 81.5 Albuminoids or flesh-formers, 3.9 Starches and sugars, 10.6 Fat 3.0 Salt (NaCl), 0.7 Phosphates, potash salts, etc., 0.3 AN IDEAL RATION WITH SOLID FOOD. — (Mrs. E. H. Richards.) Material. Amount. Proteid. Fat. Carbo- hydrates. Calories. Gm. Ozs. Gm. Ozs. Gm. Ozs. Gm. Ozs. Bread, .... 453-6 16 31-75 1. 12 2.26 O.08 257.28 9.04 1,206.82 Meat, .... 226.8 8 34.02 1.20 11-34 0.04 243.72 Oysters, . . . 226.8 8 12.52 O.44 2.04 O.07 70.01 Breakfast cocoa, 28.3 1 6.60 O. 23 7 - 5 o 0. 26 9.60 °-34 135-42 Milk 113 4 4 363 O.I3 4.42 O.16 4.88 1 o-i 7 75-55 Broth, . . . . j 453-6 16 18.14 O.64 18.14 0.64 90.72 3.20 613.21 Sugar, . . . . 1 28.3 1 27-36 0.96 112.17 Butter, . . . j 14.17 0.14 12.27 118.62 Total, . . 57-97 • 389.84 2 , 575-52 The following table is a fair average work ration in round num- bers, based on such data as those in the other tables : ESTIMATED WORK RATION, MAXIMUM AND MINIMUM.— (Mrs. E. H. Richards.) Proteid, gm., . . . Fat, gm. , . . . Carbohydrates, gm., Calories, .... For One Day. } 125 ' \ no f 125 • \ 90 J 450 ' \ 450 / 3 > 5 °° • • \ 3,000 About 30 gm. 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. For One Day. Proteid, gm., 75 Carbohydrates, gm. , ... 325 Fat, gm., 40 Calories, 2,000 226 ENERGY PRODUCED BY FOODS. It will be observed that the totals are somewhat less in this diet than those of the preceding 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 oxidized in the body: Food Stuff. With Usual Percentages of Water. One Ounce Water Free. Beef (best quality), uncooked, Foot -tons. 48.5 Foot-tons. 199 Meat (served to soldiers), uncooked, 57.8 243 Beef (fattened), uncooked, 96.0 280 Meat, cooked, 102.6 240 Corned beef (Chicago), 124.0 217 Salt beef, 52.0 138 Salt pork, 71.6 166 Fat pork, 202.0 336 Dried bacon, 292.3 346 Smoked ham, 179.6 267 Whitefish, 44-3 209 Poultry, 50.7 204 Bread, 87.5 147 Wheat-flour, 123.6 146 Biscuit, 173-3 189 Rice, 126.5 141 Oatmeal, 130.0 154 Maize, 132.0 160 Macaroni, 122.7 146 Millet, 125.9 I49 Arrowroot, 1 16.4 138 Peas (dried), 118.9 151 Potatoes, 33 -° I 4 I Carrots, 14-3 137 Cabbage, 13.0 158 Butter, 344-5 367 Eggs 67.3 265 Cheese, 149.9 245 Milk (cows’), new, 26.9 225 Cream, 109.2 365 Skimmed milk, 20.4 181 Sugar, 126.4 128 Pemmican, Ale (Bass’s bottled), 270. 1 293 30.0 260 Stout (Guinness), 41-5 360 Professor Egleston’s standard of nutrition is high. He places the daily allowance of nutritive material at 700 gm., divided as fol- lows : Carbohydrates, 400 gm. ; fats, 150 gm.; proteid, 150 gm., — yielding in all 3650 calories. FOOD VALUES OF EDIBLE PORTIONS OF DIET. 227 PERCENTAGE COMPOSITION OF EDIBLE PORTIONS OF GARRISON RATION . — ( Captain C. E. Woodruff \ M. D . , Assistant Surgeon, U. S.A.) Water. Protein. Fats. Carbo- hydrates. Salts. Energy Calories, PER LB. Bacon, fat, 20.0 8.00 69- 5 2-5 3,080 Beans, 12.6 23.10 2.0 59-2 3-1 1,615 Pork, salt and fat, . . . 12. 1 0.90 82.8 4.2 3,510 Sugar, ground, .... 2.0 97-8 0.2 1,820 .Sugar, brown issue, . . 3-0 96.5 0-5 L795 Flour, 12.5 1 1. 00 1.0 74-9 o-5 1,644 Beef, 55-o 17.10 27.0 0.9 1,460 Potatoes, 78.9 2.10 0.1 17.9 1.0 375 Onions 87.9 1-4 o-3 10. 1 0.6 225 Oatmeal, 7.6 15. 10 7-i 68.2 2.0 1,850 Cornmeal, 150 9.20 3-8 70.6 1.4 1,645 Canned apples, .... 83.2 0. 20 0.4 . 15-9 0.3 3i5 Dried apples, .... 25.0 0.90 1.8 7i-5 1.4 1 ,418 Tapioca or corn -starch, 2.0 97.8 0.2 1,820 Butter, 10.5 1. 00 85.0 o-5 3-0 3,6i5 Syrup, 43-7 55-o 2-3 1,023 Lard, 12.0 0.60 83-4 4.0 3,57o Rice, 12.4 7-4 0.4 79-4 0.4 1,630 Canned corn, 81.3 2.80 1. 1 13.2 0.6 345 Canned tomatoes, . . . 96.0 0.80 0.4 2-5 o-3 80 Macaroni and vermicelli, 131 9.00 o-3 76.8 0.8 1,406 Milk, fresh, 14. 1 0.843 0.802 1.069 0.164 418 Milk, condensed, . . . 25.0 17.00 11. 0 44.00 3-o L595 Peas, 12.3 26.70 1-7 56.40 2.9 1,565 Raisins, 40.0 0.40 24.00 0.6 440 Cheese, 35-o 33 00 22.0 5.00 5-o 1,600 Prunes, 3°° 2.50 12.0 0.6 140 Cabbage, 92.0 2.10 0.6 5-5 1. 1 i55 Ham, 41.5 16.7 39- 1 2.7 1,960 Apricots, canned, . . 50.0 2.00 30.0 0.6 460 Barley, 13.00 2.7 76.0 3-° 1,800 Chocolate, 12.0 20.00 50.0 10. 0 4.0 2,650 Sausage, 41.2 13.80 42.8 2.2 2,065 Oysters, 87.1 6.00 1.2 3-7 2.0 230 Salmon, canned, . . . 63.6 21.60 13-4 1.4 965 Crabs, 15.0 1.0 526 Crackers, 10.3 9-4 70.5 1,900 Church furnishes the following table showing the number of tons which it is calculated could be raised 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 develop work, the rest going into heat production : I pound beef-fat raises 5,649 tons ] [ foot high. I pound oatmeal “ 2,439 “ “ “ I pound gelatin “ 2,270 “ “ “ 1 pound lean beef “ 885 “ “ “ I pound potatoes “ 618 “ “ “ impound milk “ 390 “ “ “ 1 pound ground rice “ 2,330 “ “ “ 228 DIETETIC KITCHEN. CHAPTER II. DIETETIC KITCHEN.— DIET LISTS. In the following pages we give the diet orders of Penzoldt, which agree essentially with those mentioned by Leube, but have this advantage over the latter, that they contain at the same time the permissible quantities of each article of food, and are also ex- panded in other directions. The following diet list, consisting of four different kinds of diet, is, like that of Leube, especially intended to be a basis for a mild dietetic treatment in cases of diseases of the stomach in general (the so-called ulcer cure of Leube). By means of a gradual transi- tion from a very light to a stronger and richer diet, it endeavors not to tax the diseased organ in the beginning, and gradually to accustom it to increased service. It is self-evident that this diet list may not with impunity be extended in the same manner to all diseases of the stomach. According to the state of the secretion, the peristalsis, and of sen- sation, other problems concerning the diet may arise. We shall revert to the special details of the several forms of disease when we come to them. It is necessary only to give the principal rules for the chief types of diseases of the stomach in this chapter. PENZOLDT’ S DIET ORDERS FOR GRADUAL TRAINING OF THE DIGESTIVE CAPACITY. FIRST DIET (ABOUT TEN DAYS). Foods or Drinks. Largest Quantity at One Time. Preparation. Character. How to be Taken. Bouillon. 250 gm., % liter. To be made from beef. Lean, very little salt, or none at all. Slowly. Cow’s-milk. 250 gm-, X liter. Well boiled, or sterilized (Soxhlet’s ap- paratus) . Pure milk, or eventually y lime-water and milk. Eventually with a little tea. Eggs. One or two. Very soft, merely warmed or raw. Fresh. If raw, stir into the warm, not boiliug, bouil- lon. penzoldt’s diet orders. 229 Penzoldt’s Diet Orders for Gradual Training of the Digestive Capacity. — First Diet (About Ten Days) ( Continued ). Foods or Drinks. Largest Quantity at One Time. Preparation. Character. How to be Taken. Meat solution (Leube - Rosen- thal’s). 30-40 gm. See Dietetic Kit- chen. It may have only a faint odor of bouillon. By teaspoonfuls or stirred up in- to bouillon. Cakes (Albert biscuits). Six. Without sugar. Not soaked or softened, but to be well masti- cated and in- salivated. Water. Y% liter. Ordinary or nat- ural carbonated, containing a little carbonic acid (Selters), Saratoga Vichy, Londonderry Lithia, Poland. Not too cold. SECOND DIET (ABOUT TEN DAYS). Foods or Drinks. Largest Quantity at One Time. Preparation. Character. How to be Taken. Calf’s-brain. 100 gm. Boiled. To be freed from all membranes and fiber. Preferably in the bouillon. Sweetbread (thymus gland). 100 gm. Boiled. Similar to above, especially to be peeled carefully. Similarly to above. Pigeons. One. Boiled. Only young ones, without skin, tendons, and the like. Similarly to above. Chickens. One, the size of a pigeon. Boiled. Like above (no fattened chick- ens). Similarly to above. Raw beef. 100 gm. Finely chopped or scraped, with a little salt. To be taken from the fillet (tender- loin). To be eaten with crackers. Raw beef sau- sage. 100 gm. Without addi- tions. A little smoked. Similarly to pre- ceding. Tapioca. 3 ° gm- Cooked to a homogeneous gruel with milk. 23O DIETETIC KITCHEN. Penzoldt’s Diet Orders for Gradual Training of the Digestive Capacity ( Continued). THIRD DIET (ABOUT EIGHT DAYS). Foods or Drinks. Largest Quantity at One Time. Preparation. Character. How to be Taken. Pigeon. One. To be fried with fresh butter, not too much. Only young ones, without skin, etc. Without sauce. Chicken. One. Like above. Like above. Like above. Beefsteak. 100 gm. With fresh but- ter, half raw (English). The meat from the fillet, or ten- derloin, well pounded. Like above. Ham. 100 gm. Raw, scraped fine. Smoked, not strong, without bones, the so- called “ Lachs- schinken.” With wheat bread. French roll, toast, or Freiberg pretzel. 5 ° gm. Baked crisp. Stale (rolls and the like). To be chewed very carefully and to be well salivated. Potatoes. 5 ° g m - a. As puree, be- ing forced through a strainer. b. As salt pota- toes, mashed. The potatoes must be mealy, crumbling when mashed. Cauliflower. 50 gm. To be cooked in salt water as vegetables. Only the “ flow- ers ” to be used. FOURTH DIET (ABOUT EIGHT TO FOURTEEN DAYS). Foods or Drinks. Larcest Quantity at One Time. Preparation. Character. How to be Taken. Venison. IOO gm. Roast. Saddle, hung, not gamy, without high flavor. Partridge. One. Roast, without lard. Young birds, with skin, tendons, feet, etc., re- moved, after having hung in pure cold air for twenty-four hours. DIET LISTS. 23I Penzoldt’s Diet Orders for Gradual Training of tiie Digestive Capacity. — Fourth Diet (Ahout Eight to Fourteen Days) ( Continued ). Foods or Drinks. Largest Quantity at One Time. Preparation. Character. How to be Taken. Roast beef. IOO gm. Fried until red. From well-fed cattle, pounded. Warm or cold. Fillet. IOO gm. In same manner as the above. In same manner as the above. In same manner as the above. Veal. IOO gm. Roast. Saddle or leg. Finely cut. Pike. 1 Perch-pike. | Carp. Trout. J 100 gm. Boiled in salt water without any additions. Carefully remove the bones. In fish sauce. Caviar. 5 ° gm. Raw. Russian caviar with but a little salt in it. Asparagus. 50 gm. Boiled. Soft, without the hard portions. With a little melted butter. Rice. 50 gm. As gruel, forced through a strainer. Soft, boiling rice. Likewise. Poached eggs. Two eggs. With a little fresh butter. With salt. Omelette souffle (Auflauf). Two eggs. With about 20 gm. sugar. Must rise well. To be eaten at once. Stewed fruits. 5 ° gm. Fresh boiled, forced through a strainer. Freed of all skins and seeds. Red wine. 100 gm. Light, pure Bor- deaux, or reli- able California. Or any similar kind of pure red wine. Slightly wanned. All of these foods should be prepared according to directions given in the “ Dietetic Cooking.” DIET LIST OF EWALD FOR CHRONIC GASTRITIS. 8 a. m. — 150 to 200 gm. of tea, with 100 gm. of stale wheat bread, toast, or zwieback. 10 a. m. — 50 gm. of wheat bread, 10 gm. of butter, 50 gm. of cold meat or ham, and either one glass of light wine or Y of a liter of milk. 2 p. m. — 150 to 200 gm. of water, milk, or bouillon of white meats; 100 to 125 gm. of meat or fish, 30 to 100 gm. of vegetables, 80 gm. compote. 4.30 p. m. — of a liter of warm milk, chocolate, or one-half milk and one- half coffee. 7 to 8 P. m. — 300 gm. of soup, 50 gm. of wheat bread, 10 gm. of butter. 10 p. m. — Occasionally 50 gm. of wheat bread, biscuit, oT zwieback ; one cup of coffee. 232 DIETETIC KITCHEN. Boas gives two lists ; the following contains the better and richer diet : Calories. 8 A. M. — 200 gm. of milk, with 40 gm. of cocoa and 30 gm. of sugar, . . 462 50 gm. of cakes, or 50 gm. of zwieback, either one, 187 10 a. m. — 50 gm. of wheat bread with 30 gm. of butter, 343 100 gm. of calf ’s-brain (or 100 gm. of sweetbread, 90 calories), . . 140 Or 100 gm. of broiled pike, 71.75 calories. 12 m. — Soup of 30 gm. of tapioca, 10 gm. of butter, 1 egg, 282 100 gm. of noodles, 352 Or 100 gm. of spinach, 165 calories; 100 gm. of bean puree, 193 calories ; 100 gm. of carrots, 40 calories ; 50 gm. of potato puree, 63.7 calories. 100 gm. of breast meat of young chicken, 106.4 100 gm. of veal cutlets (250 calories), or, in its place, 100 gm. of broiled veal, pigeon, venison, or fish. 100 gm. of farina or omelette, or egg-pancake, 288 3 p. m. — 100 gm. of milk, with 20 gm. of sugar, flavored with tea, . . . 147 25 gm. of cakes, 93.5 7 p. m. — 50 gm. of wheat bread, 130 gm. of butter, 343 50 gm. of scraped raw beef, 459-5 3203.4 HEMMETER’S DIET LIST FOR CHRONIC GASTRITIS WITH UNIM- PAIRED MOTILITY AND INTESTINAL DIGESTION. Also Available for Lowered Nutrition where Intestinal Functions are Normal. 7.30 A. M. — If the bowels are regular, ]/ 2 of a pint of hot normal saline solution. If the bowels are constipated, a pint of cold Saratoga Vichy, Bedford Magnesia Spring, or plain cold water. Calories. Breakfast, 8 a. m. — 3 ounces or 100 gm. of farina, boiled with milk, . 127 Or 100 gm. of cerealin, boiled with milk; Or 100 gm. of breakfast wheat (strained), boiled with milk. Calories. One soft-boiled egg 80 Two ounces of wheat bread, toasted, 156 One ounce of best fresh butter, 212 One cup of wheat coffee (made of 100 gm. of roasted choice wheat, 250 c.c. of boiling water, and 1 50 gm. of milk). Instead of this the same portions of tea and milk or cocoa can be used, . . . 100 Sugar, 10 gm. (2^ drams), 40 The farina or cerealin will taste better if eaten with a roasted apple. As the digestive power improves, the egg is served in form of omelette, or poached, on toast. DIET LISTS. 233 Calories. 10.30 A. m. — 100 gm. of scraped ham (3^ ounces) 120 30 gm. of crackers or toast (one ounce), 107 226 gm. or eight ounces of broth. Instead of broth, milk, kefyr, and matzoon may be permitted in the same quantity, .... 306 Dinner, i p. m. — Soup made of 250 gm. or eight ounces of bouillon, 30 gm. or one ounce of rice or tapioca, 10 gm. or 2 ]/z ounces of butter, and one egg, 282 In case of much weakness and emaciation, y 2 of a tablespoonful of somatose should be added. The patient must not be aware of the addition of artificial foods. Calories. 120 gm. of breast meat of broiled fowl, 228 Or scraped tenderloin formed into patties and broiled ; Or steamed or broiled bluefish, trout, white or yellow perch ; Or broiled rockfish or sweetbreads. 50 gm. or two ounces of potato puree, 637 100 gm. or 3 )/$ ounces of carrots, steamed, 40 Or 100 gm. of puree of beans or peas ; Or 100 gm. of strained tomato puree. 100 gm. of finely divided spinach. One cup custard made of two eggs, 160 Or, instead of this, 100 grs. of sherry gelatin, or stewed apples, or plums, or rice in form of very light pudding made with slices of apple, no raisins. One glass (100 gm. or 3 ounces) of Hungarian Tokay ( J. Palug- yay & Sons, Pressburg), 50 This list is made intentionally abundant in order to permit of latitude in making a selection. 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 bouil- lon, and a separate sauce is made and flavored with scraped sar- delles. Calories. 3 p . m . — One cup of chocolate made with 30 gm. or 1 ounce of breakfast cocoa, or v. Mehring’s Kraft-chocolate, and yi of a pint of milk, 135.5 30 gm. of crackers, coffee-cake without grated nuts, cinnamon shortcake with but the faintest trace of cinnamon, 107 If the sweet chocolate is not agreeable, plain milk, or a glass of light Rhine wine with crackers, is allowable. Coffee in small quantities may'' be added to the milk at this hour. 16 234 DIETETIC KITCHEN. Calories. Supper, 6.30 p. m. — Broiled, panned, or raw oysters, 240 gm. or eight ounces, 70 If there is sub- or anacidity, the addition of a little grated horse- radish, lemon-juice, or catsup to the raw oysters should not be forbidden. Crackers, two ounces or 60 gm., 107 Butter, one ounce or 30 gm 212 ]/ 2 of a pint of reliable Rhine wine, 50 Or y 2 of a pint of imported beer, or y z of a 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. Note. — If the gastritis is evidently due to abuse of alcohol, the wines and beer must be excluded. BILL OF FARE FOR CHRONIC CATARRH OF THE STOMACH, WITH THE DIGESTION OF THE STOMACH ONLY, REDUCED. — ( Wegele.) Albumin. Fat. Carbo- hydrate. Alcohol. Morning : 150 gm. of pepton cocoa, 8.00 6.0 7-50 25 gm. of butter (on toasted roll), . 0.18 20.8 0.15 Forenoon : 1 soft egg, 6.00 5-0 Noon : 200 gm. of oatmeal soup, 12.50 0-3 18.00 150 gm. of fowl, 28.00 I 3-5 I.80 200 gm. of carrot, 2.14 0.4 16.30 Afternoon .- 150 gm. of pepton cocoa, 8.00 6.0 7 -So 25 gm. of butter and Albert biscuit or banquet crackers, O.18 20.8 0.15 Evening : 1 e gg> 6.00 5 -o 100 gm. of scraped ham, .... 25.00 8.0 100 gm. of macaroni, with toasted bread crumbs, 9.00 0.3 76.70 During the Day : 200 gm. of wine, 6. co 16.0 75 gm. of toast, 9.00 * i -5 63.90 Total, 117.20 94.6 236.01 16.0 Calories, about 480 890 | 970 IOO Entire combustion value about 2440 calories. DIET LISTS. 235 BILL OF FARE FOR ATROPHIC CATARRH.— ( Wegele-Penzoldt.) Albumin. Fat. Carbo- hydrate | Alcohol. Morning : 150 gm. of maltoleguminose cocoa, . 6.00 4.00 ' 3-50 Forenoon : 150 gm. of wine, 20 gm. of butter (on toasted bread), 4.00 12.0 0.15 16.60 0. 12 Noon : 100 gm. of maltoleguminose soup, . 2.60 O.IO 6.20 loo gm. of scraped beefsteak, . . . 20.00 6.00 100 gm. of mashed potatoes, . . . 3. 10 0.50 21.30 10 gm. of malt extract, 0.50 5 - 5 ° Afternoon : 1 cup of tea (with toast), 20 gm. of butter, 0.15 16.60 0. 12 30 gm. of honey, 0.40 22.00 Evening : 250 gm. of rice mush, 22.00 8.25 71.00 During the Day : 75 gm. of toast (or toasted bread), . 9.00 I.50 63.90 10 o’clock at Night : 250 gm. of milk, 8.70 9-30 12.00 10 gm. of cognac brandy, .... ... 7.0 Total, 72.70 62.85 219.64 19.0 Calories, about 3 °° 580 920 13 ° Entire combustion value about 1930 calories. BILL OF FARE FOR ATONY OF THE STOMACH, WITH GASTRIC DIGESTION REDUCED. — ( Wegele ) Albumin. Fat. Carbo- hydrate. Alcohol. Morning : 150 gm. of leguminose cocoa, . . . 6.0 4.0 13-5 50 gm. of cream, 1.8 13-3 1.8 Forenoon : 1 soft egg, 6.0 5 -o 20 gm. of toast, 2 -5 0.4 15.0 Noon : 100 gm. of scraped beefsteak, . . . 17. 1 6.0 200 gm. of mashed potatoes, . . . 4.2 2.7 42.6 20 gm. of malt extract, 1.0 11. 0 Afternoon : 150 gm. of leguminose cocoa, . . . 6.0 4.0 13-5 50 gm. of cream, 1.8 13-3 1.8 Evening: 250 gm. of tapioca pulp, 12.0 8.0 11. 0 15 gm. of diastase malt extract, . . 0.8 9.0 236 DIETETIC KITCHEN. Bill of Fare for Atony of the Stomach, with Gastric Digestion Reduced. — ( Wegele') ( Continued ). Albumin. Fat. Carbo- hydrate. 1 Alcohol. During the Day : 50 gm. of toast, 6.0 1.0 35 -o 10 o’clock at Night: 200 gm. of milk, IO gm. of cognac, 6.4 7.2 9.6 6.9 Total, 71.6 64.9 163.8 | 6.9 Calories, about 290 600 670 50 Total combustion value about 1610 calories. At noon, of course, other kinds of meat could be chosen, such as fowl or game; likewise at night rice or thick gruel. With fermentation of the stomach, however, the following bill of fare had best be used after a few days : Morning : 100 gm. of scraped ham (can) or smoked meat, and 20 gm. of bread crust. Forenoon : One soft egg and 20 gm. of bread crust or toast. Noon : 100 gm. of scraped beefsteak and scrambled eggs (two). Afternoon : Same as forenoon. Evening : Same as noon. Two clysters of y 2 to 1^ per cent, common salt solution. HEMMETER’S DIETARY FOR ANACID DILATATION. Calories . 7.30 A. m. — Lavage with NaCl solution, or a decinormal solution of HC 1 . 8 A. M. — Cerealin with cream, 150 gm., 395 Mosquera beef chocolate, 200 gm., 140 Malt extract, 10 gm., 24.5 10 A. m. — Toast or aleuronat bread (see dietetic directions), 60 gm., . . 135 Butter, 20 gm., 163 12 m. — Boiled round of beef, 150 gm., 440 Mashed potatoes, 50 gm., 63 Spinach or carrots, 100 gm 165.5 In place of these, purees of peas, beans, lentils, or turnips are allowed. Omelette souffle, 100 gm 244 3 P. M. — 100 gm. of tea, 50 gm. of Albert biscuits, 10 gm. of milk, . . . 254 DIET LISTS. 237 Calories. 7 p. M. — 100 gm. of scraped ham in omelette, 244 Or 60 gm. of scraped ham (262 calories). 200 gm. of farina with milk, 432 60 gm. of toast, 20 gm. of butter 298 9.30 P. M. — Milk, 300 c.c., 202 Two ounces of banquet crackers or Albert biscuits 200 Or in place of the milk a glass (two ounces) of approved Tokay or Malaga. BILL OF FARE FOR ATONY OF THE STOMACH, WITH THE PRODUCTION OF HYDROCHLORIC ACID SUSTAINED OR INCREASED. — ( Wegele.) Albumin. Fat. Carbo- hydrate. Alcohol. Morning: 150 gm. of pepton cocoa, 8.0 6.0 7-5 j 50 gm. of cream, 1.8 13-3 1.8 Forenoon : 30 gm. of French roll, 3-o . 0.2 20.0 50 gm. of ham, 12.5 4.0 1 e gg, 6.0 5-0 Noon : 120 gm. of roast meat, 21.0 8.0 200 gm. of mashed potatoes, .... 4.2 2.7 42.6 Afternoon : 150 gm. of pepton cocoa, 8.0 6.0 7-5 50 gm. of cream, 1.8 13-3 1.8 Evening : 120 gm. of cold roast meat, .... 21.0 8.0 200 gm. of rice, 9.0 6.6 '28.6 IO O’CLOCK : 100 gm. of wine, . 3-3 7.8 During the Day: 50 gm. of toast 6.5 1.6 41.0 Total, 102.8 74-7 I 59- 1 7.8 Calories, about 420 700 640 55 Total combustion value about 1815 calories. Instead of ham, caviar and butter with slices of toasted roll, or scrambled eggs with smoked meat, may be given in the forenoon. At noon, beefsteak, fillet, game, or fowl are allowed, and for side dishes some mashed carrots or spinach. At night, calf’s-foot jelly and omelette souffle. In convalescence, 10 to 15 gm. of condensed milk or malt extract three times daily after meals can be prescribed, through which the nutritive value of this diet is considerably increased. 238 DIETETIC KITCHEN. BILL OF FARE FOR ENLARGEMENT OF THE STOMACH WITH STENOTIC APPEARANCES. — ( Wegele.) Albumin. Fat. Carbo- hydrate. Alcohol. Morning : 100 gm. of scraped ham, 25.0 8.0 Tea with 50 gm. of cream, 1.8 13-3 ‘ 1.8 Forenoon : 2 eggs, 20 gm. of sugar, 12.0 10.0 16.0 *13-8 10 gm. of cognac, Noon : 100 gm. of scraped beefsteak, . . . 20.7 i-5 100 gm. of mashed potatoes, .... 3-1 o -5 21.3 Afternoon : Tea with 50 gm. of cream, 1.8 13-3 1.8 Evening : 100 gm. of roast chicken (hashed) , . 20.7 i-5 100 gm. of flour puff-paste, 4.2 4-3 22.0 During the Day : 80 gm. of toast, 8.5 1.2 55-o Night : 200 gm. of milk, 6.4 7.2 9.6 Total, 104.2 60.8 127.5 13.8 Calories, about 427 565 722 100 Total combustion value about 1814 calories. With this bill of fare it is most difficult to have a variety. Beef- steak scraped fine from lean meat, chicken, pigeon, lean ham, smoked meat, cold roast beef, and fillet are recommended. In the evening one may often serve also calf’s-foot jelly, tapioca, or milk jelly. With occasional improvement condensed milk, cream, malt extract, and milk jellies may be tried by spoonfuls between meals. Besides these a nutritive clyster (following a cleansing enema) is to be given twice a day in these severe cases. With pronounced stenosis, prompt operation is necessary ; where this is impossible or refused, rectal feeding is preferable to feeding by the stomach. One may waive the somewhat tedious meat-pancreas clysters, when a considerable quantity of meat is taken in per os, and employ either Ewald’s or Boas’ method of rectal alimentation, since accord- ing to the investigations of Eichhorst (“ Pfluger’s Archiv,” Bd. iv, 1871), Ewald (“ Zeitschrift f. klin. Med.,” Bd. xii, 1887), and Huber (“ Deutsch. Archiv f. klin. Med.,” Bd. xlvii), the digestion of the albumen of eggs and milk proceeds very well without previous DIET LISTS. 239 peptonization in the rectum, while it is considerably increased by the addition of common salt (one gm. to one egg) (see chapter on Rectal Alimentation). Boas (“ Diagnostik und Therapie der Magen- krankheiten,” zweite Aufl., 1891, S. 244) has followed out rectal nutrition for ten to fourteen days, in cases of severe gastrectasia with symptoms of fermentation, and attained not only the disap- pearance of the symptoms of fermentation and a considerably better general state of health, but also temporary increase in weight, — a success which lasted from three to four months. If to the preceding bill of fare two more nutritive clysters are added, the patient receives : Albumin. Fat. Carbo- hydrate. Alcohol. 4 eggs, 100 gm. of red wine, 20.0 24.O . . . 3-3 ‘7.V Total, 20.0 24.O 3-3 7.8 Calories, 82 224 3 i 54 Total combustion value about 391 calories. If we assume that of this only ten gm. of albumen, two gm. of carbohydrate, ten gm. of fat, and four gm. of alcohol should attain resorption, we would obtain a total combustion value of about 175 calories. With two nutritive clysters, according to Boas, the following increase would be attained : Albumin. Fat. Carbo- hydrate. Alcohol. 500 gm. of milk, 17.0 18.2 24.2 4 eggs, 30 gm. of red wine, 40 gm. of leguminose flour, 24.0 20.0 2.0 8.8 3-6 25.0 Total, 49.8 41.8 49.2 2.0 If half be assumed as resorbed, then there would be an addition of about 25 gm. of albumin, about 20 gm. of fat, about 25 gm. of carbohydrate, about one gm. of alcohol. This would give a total combustion value of about 1850 calories (Wegele). 240 DIETETIC KITCHEN. BILL OF FARE FOR GASTRIC CARCINOMA WITHOUT PERCEPTIBLE STENOTIC APPEARANCES. — ( Wegele.) Albumin. Fat. Carbo- hydrate. • Alcohol. Morning : 150 gm. of maltoleguminose cocoa, . 6.0 4.0 13-5 Forenoon : 200 gm. of kefyr, 6.6 4-5 3-8 Noon : 150 gm. of maltoleguminose soup, . . 4.0 0.15 9-3 100 gm. of scraped beefsteak, . . . 20.0 6.0 Afternoon : 150 gm. of maltoleguminose cocoa, . 6.0 4.0 13-5 Evening : 100 gm. of scraped ham, 25.0 8.0 8.0 150 gm. of tapioca, 7.0 5-o 10 O’CLOCK : 200 gm. of kefyr, 6.6 4-5 3-8 With the cocoa, 30 gm. of honey, . . With the kefyr, 20 gm. of cognac, . . 0.4 22.0 14.0 During the Day : 50 gm. of toast, 6.6 1.0 35-o Total, 87.6 37-i 108.9 15.0 Calories, about 360 35o 45o 100 Total combustion value about 1260 calories. For a change, tea may be often given instead of cocoa ; where lcefyr does not agree with the patient, or is refused by him, one may try condensed milk with cognac instead ; further, one may let him eat butter upon toast, or toasted bread with the tea, and also have variety in the meats, so long as the appetite for them remains. Naturally, in the last stages a considerable narrowing of the list, both in quantity and quality, takes place, and one must make the greatest concessions to the individual tastes of the patient. In the morning either cocoa or tea, with slices of toasted roll spread with meat extract or caviar ; then allow a little wine with one soft egg, or egg with cognac and sugar, or a glass of champagne ; at noon sweetbread in soup, smoked ham, pickled meat, smoked meat (which foods are more difficult of decomposition), gruel, rice, mondamin cooked in milk, according to taste. In the afternoon, tea with cognac or cocoa, and in the evening calf ’s-foot jelly, or meat-extract jelly, or meal soup will be suitable. In addition, the nutritive clysters mentioned above. (A more detailed calculation of the diet at this stage has little value, and is therefore omitted.) DIET LISTS. 24I (I) BILL OF FARE FOR CURE OF ULCER (TO BE KEPT UP AT LEAST TEN DAYS). — [Leube- Penzoldt- Wegele.) Albumin. Fat. CARBO- HYDRATE. Morning : 250 gm. of milk, 8.50 9.00 12.0 Two cakes (5 gm. each), I.IO 0.50 7-3 IO O’CLOCK : 250 gm. of milk or bouillon, 8.50 9.00 12.0 One cake, 0.60 0.25 3-7 12 O’CLOCK : 150 gm. of bouillon, 0-75 0-45 0.9 50 gm. of meat solution (or one egg), 8.50 3.00 3-5 4 o’clock : 250 gm. of milk, 8.50 9.00 12.0 Two cakes, 1. 10 0.50 7-3 150 gm. of bouillon, o -75 0-45 0.9 50 gm. of meat solution (or one egg), . . . . 8.50 3.00 3-5 Two cakes, 1. 10 0.50 7-3 Total, 47-9 35-65 70.4 Calories, about 200 330 330 Total combustion value about 860 calories. (2) BILL OF FARE FOR CURE OF ULCER (TO BE KEPT UP AT LEAST SEVEN DAYS) . — {Leube- Wegele.) Albumin. Fat. Carbo- hydrate. Morning : 250 gm. of milk, 8.5 9.00 12.0 Three cakes, 1.8 o-75 II. I 10 O’CLOCK : 200 gm. of bouillon, 3-2 4.40 3-2 One egg, 6.0 5.00 Noon : One boiled pigeon, 22.0 1. 00 0.7 About 200 gm. of rice in bouillon, 5-o 2.00 40.0 4 O’CLOCK : 250 gm. of milk, 8-5 9.00 12.0 Two cakes, 1. 1 0.50 7-3 8 O’CLOCK : 150 gm. of bouillon, 6.4 6.70 9.0 100 gm. of sweetbread, 28.0 0.40 Total, 90.5 38-75 95-3 Calories, about 370 35o 390 Total combustion value about mo calories. 242 DIETETIC KITCHEN. (3) BILL OF FARE FOR CURE OF ULCER (FOR AT LEAST FIVE DAYS).— ( Wegele.) Albumin. Fat. Carbo- hydrate. Morning : Two cups of tea or coffee, with 100 gm. of milk, 3-4 3.60 4.8 20 gm. of sugar, 0-5 18.2 Three cakes, 1.8 0-75 II. I IO O’CLOCK : 200 gm. of bouillon, 3-2 4.40 3-2 One egg, 6.0 5.00 Noon : 200 gm. of soup, 150 gm. of beefsteak, 3-2 6.00 17.0 31.0 2.20 100 gm. of mashed potatoes, 31 0.85 21.3 4 O’CLOCK : Two cups of tea with 100 gm. of milk, .... 3-4 3.60 4.8 20 gm. of sugar, o -5 18.2 Three cakes, . 1.8 0-75 II. I Evening : 100 gm. of scraped ham, 25.0 8.10 200 gm. of soup, 3-2 6.00 17.0 Total, . 86.1 41.25 126.7 Calories, about 350 380 5 20 Total combustion value about 1250 calories. (4) BILL OF FARE FOR CURE OF ULCER (TO BE KEPT UP AT LEAST ONE WEEK). ' Albumin. Fat. Carbo- hydrate. Morning : Two cups of tea or coffee, with 100 gm. of milk, 3-4 3-6 4.8 20 gm. of sugar, 0-5 18.2 One sweetbread (50 gm.), 4-5 o -5 29.0 10 O’CLOCK : 200 gm. of bouillon ‘ 3-2 4.4 3-2 One egg, 6.0 5 *° Noon: 200 gm. of soup, 3-2 6.0 17.0 150 gm. of roast fowl, 27.6 14.0 i -7 100 gm. of carrots or spinach, . 1.0 0.2 8.1 200 gm. of light flour food, 9.0 8.4 45 -o 4 O’CLOCK : Two cups of tea or coffee, with 100 gm. of milk, 3-4 3-6 4-8 20 gm. of sugar, One sweetbread, 0-5 18.2 4-5 0.5 29.0 Evening : 100 gm. of cold roast meat, 38.2 2.8 250 gm. of tapioca, 7.0 5 -o 8.0 DIET IN CHRONIC DIARRHEA. 243 (4) Bill of Fare for Cure of Ulcer (to be kept up at least one week) ( Continued). Albumin. Fat. Carbo- hydrate. 10 o’clock at Night: 250 gm. of milk, 8.5 9.0 12.0 Total, 120.5 63.0 199.0 Calories, about 495 585 815 Total combustion value about 1900 calories. Instead of tea or coffee, milk may also be served, by which the nutritive value of this diet is not inconsiderably increased. Concerning the first list it is to be remarked that instead of meat solution, eggs may be given (stirred into the soup). Further, in the second and third lists it is allowable to give two or three soft-boiled eggs instead of meat in the evening. The fourth list may, after a time, be quantitatively and qualita- tively expanded, since the following are allowed : Meats (fillet, roast beef, beefsteak, roast veal “ from the leg,” spring chicken, pigeons, partridges, venison). Fish — pike and perch (boiled) are allowable. Vegetables — mashed potatoes, spinach, and golden turnips. Of the farinaceous foods, the light puff-paste of rice, fine oat- meal, tapioca, and omelette souffle come under consideration. At evening, mushes with whisked eggs ; preserved or stewed fruits may be tried gradually. Salads are entirely to be avoided. Wines may now be permitted in small quantities before meals. By gradual increase in quantity, one must attempt to give the body the nourishment necessary for its proper maintenance. DIET LIST FOR CHRONIC DIARRHEA (Severe Cases).— ( Wegele). Albumin. Fat. Carbo- hydrate. Alcohol. Morning: 200 gm. of acorn cocoa, boiled in water, 2 -3 3.60 12.0 One soft egg, 6.0 5.00 Forenoon : 250 gm. of decoction of whortleberries (from 80 gm. of dried berries), . . 0.6 I.30 4-7 250 gm. of slimy soup, 5-5 4.00 7-5 One egg in the soup, 6.0 5.00 100 gm. of scraped meat (lean), . . . 20.7 I.50 50 gm. of rice in bouillon, .... 4.0 0.50 38.0 244 DIETETIC KITCHEN. Diet List for Chronic Diarrhea (Severe Cases). — ( Wegele) ( Continued ). Albumin. Fat. Carbo- hydrate. Alcohol. Afternoon : 250 gm. of whortleberry decoction, . 0.6 1.30 4-7 Evening : 250 gm. of maltoleguminose soup, . . 6-5 0.25 15-5 With one egg, 6.0 5.00 150 gm. of minced chicken, .... 15.0 9.00 12.0 During the Day: 75 gm. of toast, 9.0 I 50 42.5 200 gm. of whortleberry wine, . . . 7.0 17.0 10 o’clock at Night: 250 gm. of barley mush (20; 250), . 5-o 4.00 25.0 Total, 87.2 42.00 168.9 17.0 Calories, about 360 390 690 120 Total combustion value about 1440 calories. At the beginning of convalescence light flour foods are allowed at noon ; afternoon, instead of the whortleberry decoction, acorn cocoa may be substituted ; at noon, roast fowl, beefsteak, fillet, roast beef, and gradually pass over to the following list : DIET LIST FOR CHRONIC DIARRHEA (Less Severe Cases).— ( Wegele.) Albumin. Fat. Carbo- hydrate. Alcohol. Morning : 200 gm. of acorn cocoa, 2.30 3-6 12.00 With one egg, . 6.00 .5.0 Forenoon : 250 gm. of kefyr (four days old), . . 8.20 5-7 2.00 3-2 Noon : 250 gm. of soup, 5 - 5 o 4.0 7-50 With one egg, 6.00 5 -o 150 gm. of roast chicken, 28.00 10.0 I.80 200 gm. of mashed potatoes, .... 6.00 i -7 42.70 4 O’CLOCK : 250 gm. of acorn cocoa, 2.30 3-6 12.00 6 O’CLOCK : 250 gm. of kefyr, 8.20 5-7 2 . CO 3-2 8 O’CLOCK : 200 gm. of soup, 3-30 6.0 17.00 With one egg, 6.00 5 -o 100 gm. of sweetbread, 28.00 0.5 IO O’CLOCK : 250 gm. of kefyr, 8.20 5-7 2.00 3-2 DIET FOR CHRONIC CONSTIPATION. 245 Diet List for Chronic Diarrhea. (Less Severe Cases). — ( Wegele) ( Continued ). Albumin. Fat. Carbo- hydrate. Alcohol. During the Day: 75 gm. of toast or toasted bread, . . 20 gm. of butter, 250 gm. of whortleberry wine, . . . 9.00 0.15 1-5 16.6 42.50 O.I2 8-75 21.5 Total, 127.00 79.6 150.25 31-3 Calories, about .5 2 ° 740 615 210 Total combustion value about 2080 calories. After convalescence has begun, have the acorn cocoa prepared with milk; add at noon light foods; at night give milk musH for a change ; gradually increase the amount of kefyr given, and thus gradually a diet of about 2500 calories’ combustion value is reached, which is to be considered sufficient. DIET LIST FOR CHRONIC CONSTIPATION. — ( Wegele.') Albumin. Fat. Carbo- hydrate. Alcohol. Morning : Before breakfast, Bedford Magnesia Spring Water, y 2 liter. 200 gm. of milk and coffee, .... 3.20 4.40 3.20 30 gm. of butter, 0.21 24.50 0.15 30 gm. of honey, o-35 0.03 17.00 loo gm. of Graham bread, 300 gm. of buttermilk, 12.15 2.80 11.20 Noon : 200 gm. of bouillon, 1. 00 0. 60 1.20 200 gm. of mutton 23.20 50-50 O.70 300 gm. of crisped cabbage, .... 4. 20 14.40 21.60 200 gm. of plums, 0.80 II.60 300 gm. of white wine or apple cider, 9.00 24-7 Afternoon : 300 gm. of buttermilk, 12.15 2.80 11.20 Evening : 150 gm. of meat, 28.20 II. 00 0.10 30 gm. of butter 0.21 24.50 0.15 300 gm. of stewed apples, 1. 00 39.00 For the several meals, 250 gm. of Graham bread, 22.50 2.50 I25.OO After evening meal, 750 gm. of beer, . . 42.60 6.50 4.70 28.8 Total, 145-77 194.50 245.80 53-5 Calories, about 600 1800 IOOO 375 Total combustion value about 3800 calories. 246 DIETETIC KITCHEN. This list is easil) varied in accordance with above statements, and eventually it may be diminished along the entire scale, or it may be changed with regard to coexistent stomach troubles. For the rest it is to be noted that with the difficult solubility of many of the foods mentioned, and with an acceleration of digestion brought about by the diet prescribed, a considerable part of the nutriment introduced with the “ ingesta ” will be only partially turned to the best advantage. Naturally, if the chronic constipa- tion is due to real catarrh, one must prescribe less irritating food and give the softer vegetables, such as cauliflower, spinach, aspar- agus, carrots; also the legumes and preserves more in form of purees. DIET LIST FOR HYPERACIDITY.— {Boas- Wegele- Fleischer.) Albumin. Fat. Carbo- hydrate. Alcohol. Morning : 100 gm. of tea with milk, 3-4 3-6 4-8 2 soft eggs, 12.0 10.0 100 gm. of raw ham, 25.0 8.0 50 gm. of cream, 2.0 13-5 i -7 Noon : 200 gm. of aleuronat-meal soup (10 al.; 20 oatmeal ; 250 soup), . . . 10.2 i -7 8.0 150 gm. of beefsteak, 58.O 3 -o 200 gm. of mashed potatoes, .... 6.2 1.7 42.6 100 gm. of white wine, mixed with Saratoga Vichy or Biliner water, 3-5 8.0 Afternoon : 100 gm. of tea, 3-4 3-6 4.8 150 gm. of cream, 2.0 13-5 i -7 Evening : 50 gm. of cold roast meat, 60.2 4.0 2 scrambled eggs, 12.0 12.0 100 gm. of wine, 3-5 ' 8.0 For the several meals, 100 gm. of aleuronat toast, 28.3 i -5 66.7 10 o’clock at Night : 250 gm. of milk, 8.5 9.0 12.0 Total, 229.2 85.1 149.4 16.0 Calories, about 94O 790 600 112 Total combustion value about 2500 calories. With the tea a little sugar is to be allowed, and the white wine is usually to be mixed with an alkaline acidulous water not con- DIET LIST FOR HYPERSECRETION. 247 taining too much carbonic acid (such as Biliner water). When convalescence sets in, the daily amount of milk is to be increased. DIET LIST FOR HYPERSECRETION. — ( Wegele.) Albumin. Fat. Carbo- hydrate. Morning : Tea with 100 gm. of milk, 3-4 3-0 4.8 2 soft eggs, 12.0 10.0 Forenoon : 150 gm. of calf’s-foot jelly, 35 -o 17.0 1.0 Noon : 150 gm. of sweetbread in bouillon, 32.0 250 gm. of tapioca mush, 12.0 * 8.0* 11. 0 50 gm. of cream, 2.0 13-5 i -7 Afternoon : 200 gm. of milk, 6.8 6.0 9.6 Evening : 200 gm. of ham, 48.0 70.0 2 scrambled eggs, 12.0 12.0 For the several meals, 100 gm. of aleuronat toast, . . 28.3 i -5 66.7 10 p. M. : 100 gm. of milk, 6-5 6.0 10.0 During Night : 100 gm. of milk, 6-5 6.0 10. 0 Total, 218.0 147.0 104.8 Calories, about 900 1360 430 Total combustion value about 2700 calories. Of course, other meats than those mentioned above may be chosen, only the glutinous are particularly to be selected; event- ually also scraped meat, ham, etc. With convalescence go over to the preceding list. With nightly complaints in consequence of acid formation, there is to be rec- ommended, besides milk or glair-water, especially raw or hard, grated eggs, and drinking afterward of alkaline waters. Penzoldt recommends the addition of one-fourth to one-third lime-water to the milk. As concerns the power of the various foods to combine with HC 1 , the following table is based upon results obtained experiment- ally by Fleischer (“ Krankh. d. Speiserohre, d. Mag. u. d. Darms,” Wiesbaden, 1896, p. 932) : 248 DIETETIC KITCHEN. Pure HC 1 . 25 Per Cent. HC 1 . Per Cent. HC 1 . Meats, ioo gm., Combine With : Calf s-brain, boiled, 0.65 2.6 55-2 Liver pudding, 0.80 3-2 6.4 Sweetbread, boiled, 0.90 3 - 6 7.2 Mettwurst, 1. 00 4.0 8.0 Saveloy, 1. 10 4.4 8.8 Black pudding, 1.30 5-2 10.4 Pork, boiled, 1 .60 6.4 12.8 Ham, boiled, 1.80 7.2 14.4 Ham, raw, I.90 7.6 15-2 Mutton, boiled, I.90 7.6 H- 2 Beef, boiled, 2.00 8.0 16.0 Veal, boiled, 2.20 8.8 17.6 Leube-Rosenthal’s meat solution, 2.20 8.8 17.6 Other Foods. Beer, 0. 10 0.40 0.80 Milk, 0.36 1.44 2.88 Wheat bread, 0.30 1.20 2.40 Graham bread, 0.30 1.20 2.40 Black (gray) bread, 0.50 2.00 4.00 Pumpernickel, 0.70 2.80 5.60 Hand cheese 1. 00 4.00 8.00 Fromage de Brie, 1.30 5.20 10.40 Edam cheese, I.40 5.60 1 1.20 Brick cheese, I.70 6.80 13.60 Pease sausage, 1.70 6.80 13.60 Roquefort cheese, 2. 10 8.40 16.80 Swiss cheese, 2.60 10.40 20.80 Cocoa, 4. 10 16.40 32.80 The author’s personal views on the dietetic treatment of hyper- acidity and hypersecretion have been clearly stated in pages 195 to 197, on the basis of a very large number of quantitative analyses of the gastric contents of forty-two normal healthy adults. He has become convinced that proteids, such as beef, eggs, fish, etc., cause a stronger secretion of HC 1 than amylaceous foods, such as rice, sago, farina, cerealin. When the glandular layer is in a state of increased excitation it is logical to avoid proteid and albuminous food as much as possible. We have made numerous prolonged observations showing that amylaceous foods and fats can maintain the nitrogen equilibrium, and even add to body-weight when proteids are excluded. We do not wish to defend the standpoint of the vegetarian, as we generally allow a small quantity of easily digestible meat for dinner, and advise about \ liters of milk if it agrees well. The views of v. Sohlern on this question merit care- ful investigation. FATTENING CUKE FOR NEUROSES. 249 SCHEDULE FOR INTESTINAL ANTISEPSIS UY MILK DIET. Also Available in Neurasthenia, Sensory and Secretory Neuroses. — {Burkart.') First Day : 7.30 a. m. — One-half of a liter of milk and two pieces of toast (the milk is to be taken a mouthful or a spoonful at a time, ^ of a liter in one-half hour). 10 A. m. — One-third of a liter of milk and one toast. 12.30 p. m. — One plate of soup with one egg, 50 gm. of roast meat. Potato puree. 3.30 p. m. — One-third of a liter of milk and one toast. 5.30 P. m. — One-half of a liter of milk and two toasts. 8 P. m. — One-half of a liter of milk, 50 gm. of roast meat, wheat bread and butter. On the ninth day the following list is applicable : 7.30 a. m. — One-half of a liter of milk and two toasts. 8.30 a. m. — Coffee and cream, wheat bread and butter. 10 A. m. — One-third of a liter of milk and two toasts. 12 m. — One-half of a liter of milk. 1 p. m. — Soup with one egg, 100 gm. of meat, mashed potatoes, 75 gm. of stewed prunes. 3.30 p. m. — One-half of a liter of milk. 5.30 p. m. — One-third of a liter of milk and two toasts. 8 P. m. — One-half of a liter of milk, 60 gm. of meat, wheat bread and butter. 9.30 p. m. — One-third of a liter of milk and two toasts. On the fifteenth day Burkart (in a severe case of dyspepsia on hysterical basis) reached the following most ample diet list : Albumin. Fat. Carbo- hydrate. 7 A. M. 500 gm. of milk, 17.0 18.2 24.0 8 A. M. One small cup of coffee or tea, with 20 gm. of cream, 0.7 5 -o 0.7 80 gm. of cold meat, 30.8 2.0 One French roll, 4-5 o -5 29.O 20 gm. of butter, o -3 16.6 0.1 loo gm. of roast potatoes, 1.8 10.0 25.0 IO A. M. 300 gm. of milk, 10.2 10.9 14.4 12 M. 300 gm. of milk, 10.2 10.9 14.4 1 P. M. 200 gm. of soup, 2.2 30 11 . 4 200 gm. of roast meat, 76.4 5-4 200 gm. of mashed potatoes, ‘ 6.2 i -7 42.6 125 gm. of prunes, 0.4 8-3 200 gm. of flour food, . . .... 12.8 21.2 45 >° 17 250 EFFECTS OF COOKING ON FOOD. Albumin. Fat. Carbo- hydrate. 3.30 P. M. 500 gm. of milk, 17.0 18.2 24.0 5.30 P. M. 300 gm. of milk, 10.2 10.9 14.4 80 gm. of cold meat, 3°. 8 2.0 One French roll, 4-5 0.5 29.O 20 gm. of butter, 0.3 16.6 0. 1 8 P. M. 80 gm. of roast meat, 30.8 2.0 40 gm. of toast, 0.6 5-2 33-2 500 gm. of milk, 17.0 18.2 24.0 9.30 P. M. 500 gm. of milk, 17.0 18.2 24.0 20 gm. of toast, o-3 2.6 16.6 Total, 295.0 199.8 380.2 Calories, about 1200 1850 1550 Total combustion value about 4600 calories. Effects of Cooking on Food. — The practice of cooking is not equally necessary in regard to all articles of food. There are im- portant differences in this respect, and it is interesting to note how correctly the experience of mankind has guided them in this mat- ter. The articles of food which we still use in the uncooked state are comparatively few ; and it is not difficult in each case to indi- cate the reason of the exemption. Fruits which we consume largely in the raw state owe their dietetic value chiefly to the sugar which they contain ; but sugar is not altered by cooking. Salads may be regarded more as a relish for other food, and as having a quasi-medicinal purpose, rather than as a substantial source of nutriment. Milk is consumed by us, both cooked and uncooked, indifferently, and experience justifies this indifference ; for Sir William Roberts found, on trial, that the digestion of milk by pancreatic extract was not appreciably hastened by previously boiling the milk. In the author’s experiments boiled milk was digested slower than unboiled milk by pancreatic juice of the dog. This eminent writer characterizes our practice in regard to the oyster as being exceptional and furnishing a striking example of the general correctness of the popular judgment on dietetic ques- tions. The oyster is almost the only animal substance which we habitually, and by preference, eat in the raw or uncooked state ; and it is interesting to know that there is a sound physiological CHEMICAL CHANGES PRODUCED BY COOKING. 25 I reason at the bottom of this preference. The fawn-colored mass which constitutes the dainty of the oyster is its liver, and this is little else than a heap of glycogen, or animal starch. Associated with the glycogen, but withheld from actual contact with it during life, is its appropriate digestive ferment — the hepatic diastase. The mere crushing of the dainty between the teeth brings these two bodies together, and the glycogen is at once digested, without other help, by its own diastase. The oyster in the uncooked state, or merely warmed, is, in fact, self-digestive. But the advantage of this provision is wholly lost by cooking, for the heat employed immediately destroys the associated ferment, and a cooked oyster has to be digested like any other food — by the consumer’s own digestive powers. With regard, however, to the staple articles of our food, the practice of cooking them beforehand is universal. In the case of the farinaceous articles cooking is actually indispensable. When men under the stress of circumstances have been compelled to sub- sist on the uncooked grain of the cereals, they have soon fallen into a state of inanition and disease. By the process of cooking, the starch of the grain is not only liberated from its protect- ing envelopes, but it undergoes a chemical change by which it is transformed into the gelatinous condition, which facilitates the action of the diastatic ferments. A change of equal impor- tance seems to be induced in the proteid matter of the grain. Sir William Roberts found that the gluten of wheat was much more digestible by both artificial gastric juice and by pancreatic extract in the cooked than in the uncooked state. In regard to meat the advantage of cooking consists chiefly in its effects on the connec- tive tissue and the tendinous and aponeurotic structures associated with muscular fiber. These are not merely softened and disinte- grated by cooking, but are chemically converted into the soluble and easily digested form of gelatin. Sir William Roberts made in- structive observations on the effects of cooking on the contents of the egg. The change induced on egg-albumen by cooking is very striking. For the purpose of testing this point he employed a solution of egg-albumen made by mixing white-of-egg with nine times its volume of water. This solution, when heated in the water- bath, does not coagulate nor sensibly change its appearance, but its behavior with the digestive ferments is completely altered. In the raw state this solution is attacked very slowly by pepsin and acid, and pancreatic extract has almost no effect on it ; but after being 252 THE PALATE A SKILFUL GUIDE. cooked in the water-bath the albumin is rapidly and entirely digested by artificial gastric juice, and a moiety of it is rapidly digested by pancreatic extract.* Indications of the Palate. — Sir William Roberts (“ Digestion and Diet”) holds that “the indications of the palate are of great importance in the regulation of diet, and should always be inquired into and carefully considered. The palate is placed like a dietetic conscience at the entrance gate of food, and its appointed function is to pass summary judgment on the wholesomeness or unwhole- someness of the articles presented to it. It acts under the in- fluence of a natural instinct, which is rarely at fault. This instinct represents an immense accumulation of experience, partly acquired and partly inherited. It is, of course, not infallible — no instinct is ; but so close and true are the sympathies of the palate with the stomach and the rest of the organism that its dictates are entitled to the utmost deference as those of the rightful authority in the choice of food. I am, of course, aware that the palate — or, rather, the civilized palate — is not always credited with these solid, good qualities. Some persons there are, not medical authorities, who distrust its office and regard its indications with suspicion, as if they were the suggestions of some frivolous and wanton agency, tempting men to a vain gratification of the senses, rather than as those of an honest and skilful guide in the choice of food. This puritanical view of the palate is wholly unscientific ; it moreover implies, to speak figuratively, a gross slander on a responsible and rarely endowed organ, which has performed in the past, and still performs, most difficult and most complicated functions with con- spicuous success; for who shall venture to say that, in the evolu- tion of the human animal from the short-lived, immoral, and stupid savage, with his diet of wild fruit, roots, raw flesh, and unfiltered water, to the status of civilized man, the promptings of the palate have not played an important and even indispensable part ? We are apt to forget that there is no such a thing as an absolutely good or an absolutely bad flavor to the animal palate. Sweet things are indifferent to the palate of the carnivora; and, conversely, the taste of flesh has no attraction to the herbivora. Each animal has its own gustatory standard, which is accurately adjusted to the wants of its particular economy.” * Raw egg-albumin does not require digestion and can be absorbed from the intestine as such ; in the stomach it invariably undergoes digestion by pepsin hydrochloric acid. DIETETICAL COOKING. 253 DIETETICAL COOKING .* General Remarks . — It is evident that the subtle art of cooking can be practised with advantage to those suffering from indigestion only by those who understand thoroughly the general fundamental principles of the art, and have in addition some experience therein. But if diligence, care, and cleanliness are very desirable qualities in cooking for people in good health, they become an absolute necessity for those who undertake the preparation of food for diges- tive organs whose functions are impaired. By no means should the attention be taken from the work by other matters, for in that case the care which is necessary will suffer, and the most scrupu- lous cleanliness must be applied (Wegele). It should be understood here that we have confined ourselves to the most necessary things, and have not considered the details con- cerning the arrangement of the kitchen, construction of the fire- place, the cooking utensils and fuel, food-stufifs or their adulteration ; and, further, we have not undertaken the description of complicated dishes, but have given directions for the preparation of only the simplest every-day dishes in such a way as to serve dietetical pur- poses. In this respect the advice of Penzoldt deserves considera- tion, to use vessels with protecting lids for the keeping of foods which are to be eaten later when cold. Naturally all food-stuffs must be of the best quality, for the best is just good enough for the sick. Aside from this, nothing in the slightest degree spoiled may be used in cooking for the sick. In the eulogy of the palate we have already emphasized appetizing preparation, for, as is well known, dyspeptics are easily seized by nausea, while, on the other hand, a suitable way of preparing food may stimulate the appetite. For the same reason, every after-taste due to the character of the cooking utensils or their uncleanliness is to be avoided as far as possible, and the utensils should be, wherever possible, earthen, enameled, or nickel-plated. Food must never be brought to the table too hot, for the patients are thus tempted to eat them in this state in spite of the directions of the physician, and on this account it is best to put the food on a second plate or cup. The contrary * We have availed ourselves of a large number of works in compiling this particular chapter. The name of the originator of any particular article of diet has been added to the directions given whenever it was obtainable. Of the larger works used we mention Sir William Roberts, Munk and Uffelmann (last edition by C. A. Ewald), Wegele, Biedert and Langermann, Leyden’s “ Handbuch der Ernahrungstherapie,” Gilman Thompson, Boas, Penzoldt and Stintzing’s “ Handbuch der Therapie,” etc. 254 GENERAL DIRECTIONS REGARDING COOKING. is just as injurious, and it is therefore well to prepare foods, which are subject to rapid cooling, in vessels with double bottoms, filled with hot water. Concerning the seasoning of the dishes, only a moderate use of cooking salt is allowed, and other spices are not to be used without the permission of the physician ; Wegele strictly forbids the use of citron or pomegranate skins in dietetical cooking. Water which is to be used for cool drinks should be boiled and then allowed to cool. Concerning the measures used in the following chapter, — I teaspoon equals about 5 gm., I tablespoon equals about 15 gm. , I soup plate equals about 250 gm. , I cup equals about 200 to 250 gm. , I wineglass equals about 150 gm., in which calculation naturally no attention has been paid to the specific gravity of the different substances. I. Drinks and Liquid Foods. Barley Soup (Ringer ). — To a tablespoonful of pearl barley washed in cold water add two or three lumps of sugar, the rind of one lemon, and the juice of half a lemon. On these pour a quart of boiling water, and let the mixture stand for seven or eight hours. Strain. The barley water should never be used a second time. Half an ounce of isinglass may be boiled in the water. If not needed at once, these barley preparations should be kept in the refrigerator, and warmed when required. They are unpalatable if taken cold. Rice-water, or Mucilage of Rice (Pavy ). — Thoroughly wash one ounce of rice with cold water. Then macerate for three hours in a quart of water kept at a tepid heat, and afterward boil slowly for an hour, and strain. A useful drink in dysentery, diarrhea, and irritable states of the alimentary canal. It may be sweetened and flavored in the same way as barley water. Lemonade (Pavy ). — Pare the rind from a lemon thinly, and cut the lemon into slices. Put the peel and sliced lemon into a pitcher with one ounce of white sugar, and pour over them one pint of boiling water. Cover the pitcher closely, and digest until cold. Strain or pour off the liquid. Beef-essence (Yeo). — Cut the lean of beef into small pieces and place them in a wide-mouthed bottle securely corked, and then allow it to stand for several hours in a vessel of boiling water. DRINKS AND LIQUID FOODS. 255 This may be given in teaspoonful doses to infants who can not take milk, and in larger quantities to adults. Beef-tea {Germain- See ). — Meat cut into small pieces, cold water added, and then gradually heated to 140° or 160° F. Press, strain, and flavor with salt and pepper. This is much inferior to the preparations made with hydrochloric acid. Chicken Broth {Bartholomew ). — Skin and finely mince a small chicken or half of a large fowl, and boil it, bones and all, with a blade of mace, a sprig of parsley, and a crust of bread, in a quart of water for an hour, skimming it from time to time. Strain through a coarse colander. Chicken, Veal, or Mutton Broth {Yeo). — Chicken, veal, or mutton broth may be made like beef-tea, substituting chicken, veal, or mutton for beef, boiling in a saucepan for two hours, and straining. For chicken broth the bones should be crushed and added. For veal broth the fleshy part of the knuckles should be used. Either may be thickened and their nutritive value increased by the addition of pearl barley, rice, vermicelli, or semolina. Mutton and Chicken Broths {Osier ). — Mince a pound of either chicken or mutton, freed from fat, put into a pint of cold water, and let stand in a cold jar on ice two or three hours. Then cook for three hours over a slow fire, strain, cool, skim fat off, add salt, and serve hot or cold. Such broth is much better than any manufac- tured meat preparations. Good mutton broth is difficult to make on account of the meat containing so much fat. Raw Meat Diet {Ringer ). — Use two ounces of rump steak; take away all fat, cut into small squares without entirely separat- ing the meat, place in a mortar, and pound for five or ten minutes ; then add three or four tablespoonfuls of water and pound again for a short time, afterward removing all sinews or fiber; add salt to taste. Before using, place the cup or jar containing the pounded meat in hot water until just warm. Or scrape the beefsteak with a sharp knife, and after removing all fat and tendon, if not already in a complete pulp, pound in a mortar. Flavor with salt and pepper. This may be taken in the form of a sandwich, between thin bread and butter, or mixed with water to the consistency of a cream. If preferred, the meat may be rolled into balls with a little white-of-egg, and boiled for two or three minutes, or until the outside turns gray, just long enough to remove the raw taste. Chicken Jelly {Adams ). — Clean a fowl that is about a year old, 256 DRINKS AND LIQUID FOODS. remove skin and fat ; chop fine, bones and flesh, in a pan with two quarts of water ; heat slowly, skim thoroughly, simmer five to six hours ; add salt, mace, or parsley to taste ; strain ; cool. When cool, skim off the fat. The jelly is usually relished cold, but maybe heated. Give often in small quantities. Milk-punch. — Make by adding brandy or whiskey or rum to milk in the proportion of about one to four or six parts of milk ; flavor with sugar and nutmeg ; shake well. Sherry or Brandy and Milk {Ringer ). — To one tablespoonful of brandy or one wineglassful of sherry, in a bowl or cup, add pow- dered sugar and a very little nutmeg to taste. Warm a breakfast cupful of new milk and pour into a pitcher. Pour the contents from a height over the wine, sugar, etc. The milk must not boil . Junket {Anderson ). — Sweeten with white sugar one pint of good milk. If wine is allowed, a dessertspoonful of sherry is an improve- ment. Heat to new-milk warmth, pour into a shallow dish, and stir in two teaspoonfuls of essence of rennet. This will form a slight curd. Grate a little nutmeg over it, or add a pinch of pow- dered cinnamon. Serve when quite cold. In cold weather the milk should be placed in a warm room to set. An excellent food and good substitute for milk in typhoid fever, etc. Egg-nog. — Egg-nog is made by adding the beaten yolk of egg and a little spirits to a tumblerful of milk, stirring well, adding sugar and white of the egg, separately beaten. The digestibility of both of these highly nourishing and stimulating preparations is enhanced by the addition of y 2 of an ounce of lime-water, which does not affect the taste. Egg and Wine {Ringer ). — Take one egg, y 2 of a glass of cold water, one glass of sherry, sugar, and a very little nutmeg, grated. Beat the egg to a froth with a tablespoonful of cold water. Make the wine and water hot, but not boiling; pour on the egg, stirring all the time. Add sufficient sugar to sweeten, and a very little nutmeg. Put all into a porcelain-lined saucepan over a gentle fire, and stir one way till it thickens, but do not let it boil. Serve in a glass, with crisp biscuits or sippets of toast. Milk for Pudding or Stewed Fruit {Ringer ). — Boil a strip of lemon and two cloves in a pint of milk; mix y 2 of a teaspoonful of arrowroot in a little cold milk and add it to the boiling milk; stir it until about the consistency of cream. Have ready the yolks of three eggs beaten up well in a little milk. Take the hot DIETETIC FOODS AND DRINKS. 257 milk off the fire, and as it cools add the eggs and a teaspoonful of orange-flour water, stirring it constantly till quite cool. Keep it in a very cool place until required for use. Arrowroot Blancmange {Ringer ). — Take two tablespoonfuls of arrowroot, ^ of a pint of milk, lemon, and sugar to taste. Mix the arrowroot with a little milk to a smooth batter; put the rest of the milk on the fire and let it boil, sweeten and flavor it, stirring ail the time till it thickens sufficiently. Put into a mold until quite cold. Arrowroot ( Pavy ). — Mix thoroughly two teaspoonfuls of arrow- root with three tablespoonfuls of cold water, and pour on them y 2 of a pint of boiling water, stirring well meanwhile. If the water is quite boiling, the arrowroot thickens as it is poured on, and nothing more is necessary. If only warm water is used, the arrowroot must be boiled afterward until it thickens. Sweeten with loaf-sugar, and flavor with lemon-peel or nutmeg, or add sherry, port-wine, or brandy if required. Boiling milk may be employed instead of water, and when this is done no wine must be added, as it would otherwise curdle. Oatmeal Gruel (Plain). — Two tablespoonfuls of oatmeal, one saltspoonful of salt, one scant teaspoonful of sugar, one cup of boiling water. Cook for thirty minutes; then strain through a fine wire strainer to remove the hulls, place again on the stove, add the milk, and heat just to the boiling point. Serve hot. Farina Pudding (U. S. Army Hospital Recipe for 12 Men). — Farina, y 2 of a pound; milk, two pints; water, one pint; sugar, 2 y 2 ounces; eggs, four ounces; nutmeg, y 2 of an ounce. Directions . — Put the water into a stewpan with a little salt. When it boils stir in the farina. Let it boil twenty minutes. Stir in the milk, which must be hot. Beat the eggs until they are very light ; mix the sugar with them. Stir in the eggs and sugar with the farina. Add the spice. Put it into a moderate oven and bake a half or three-quarters of an hour. Port- wine Jelly {Ringer ). — Put into a jar one pint of port-wine, two ounces of gum arabic, two ounces of isinglass, two ounces of powdered white sugar-candy, y of a nutmeg grated fine, and a small piece of cinnamon. Let this stand closely covered all night. The next day put the jar into boiling water and let it simmer until the contents are dissolved ; then strain, let stand till cold, and then cut into small pieces for use. Nutritious Coffee {Ringer ). — Dissolve a little isinglass in water, 258 DIET LISTS. and then put Y / 2 of an ounce of freshly ground coffee into a sauce- pan with one pint of new milk, which should be nearly boiling before the coffee is added ; boil both together for three minutes. Clear it by pouring some of it into a cup and dashing it back again, add the isinglass, and let it settle on the hob for a few minutes. Beat up an egg in a breakfast cup and pour the coffee upon it ; if preferred, drink it without the egg. Glair-water. — Into 200 c.c. of cold water which has previously been boiled, put with constant stirring the white of one egg, and add, according to prescription, three teaspoonfuls of powdered sugar, or grape-sugar, or 10 gm. of cognac. The white of an egg equals about 12 calories; 15 gm. of sugar equals about 50 calories ; 10 gm. of cognac equals 50 calories. Kefyr. — It is best to procure moist lcefyr mushrooms (not the dried grains) prepared for immediate use. They can be pro- cured from the Caucasian Kefyranstalt in Breslau, or from Dr. M. Lehmann, Berlin C. (43 and 44 Heiligegeist Strasse). Pour away the liquid contained in the bottle, wash the mushrooms in a luke- warm (about 1 5 0 R. or 18.7° C.) soda solution of 5 : 1000, rinse with clean lukewarm water, and after pouring off the water place the mushrooms in a vessel of porcelain or Bunglan clay of two liters’ capacity. Previously two liters of milk should have been boiled and allowed to cool again. Now pour the milk, whose tempera- ture should be about 15 0 R. or 18. 7 0 C., upon the mushrooms, close the vessel tightly, and let it stand twenty-four hours in a place whose temperature is 13 0 to 15 0 R. or 1 8.7° C. (in summer in the cellar), during which time it is expedient to often stir the milk care- fully. At the expiration of this time it should be stirred again, and the milk is then poured through a moderately fine wire sieve into thoroughly cleaned bottles with patent stoppers. These bottles are again to be kept twenty-four, thirty-six, forty-eight, or, at the highest, fifty-four hours (according as kefyr one, two, three, or four days old has been prescribed) in a place whose temperature is kept at about 15 0 R. or 18. 7 0 C., lying, not standing up, and are then ready for use. The process of fermentation may be hastened by frequent shak- ing, also with heat, on which account the fermentation takes place more quickly in midsummer, and the kefyr consequently will be finished sooner. The mushrooms which remained in the sieves after pouring off the milk into the patent flasks must each time be rinsed with lukewarm water and freed from particles of cheese, MEAT EXTRACTS, ETC. 259 and afterward placed again in the thoroughly clean porcelain ves- sel, and milk is then again poured upon them. After two or three days the preparation is so regulated that each day two bottles (of one liter each) become ready for use, for which reason four patent- stoppered bottles are necessary. Once a week the bottles must be rinsed with a lukewarm soda solution of 5 : 1000 instead of with lukewarm water, in order to free them from acid. At first let the patient drink one wineglassful two or three times a day, then l /^ of a liter, and constantly increase the quantity until the prescribed dose has been reached. One hundred gm. of kefyr equal about 45 calories. Almond Milk. — Thirty grs. of sweet almonds and two bitter almonds are blanched after they have lain twenty-four hours in cold water. One can also scald the almonds with boiling water; then they can be easily pressed out of their hulls after a few min- utes. The almonds are either ground in a mill or pounded in a mortar, then mixed with of a liter of warm water or warm milk, and the mixture is allowed to stand two hours, after which it is strained through a cloth and the juice well pressed out. Thirty grs. of almonds equal 200 calories ; 250 gm. of milk equal 170 calories. Extract of Meat ( according to Wiel), “ Succus carnis recenter expressus.” — Meat free from fat is chopped fine, arranged in sev- eral layers, which are separated by coarse (filter) linen, and sub- jected to pressure in a colander ; the juice is given pure (as medi- cine) by the teaspoonful, or also diluted with beef-tea, but must not be subjected to a temperature higher than 50° R. or 62.5° C., for otherwise the albuminous parts contained in it would coagu- late. “Valentine’s meat-juice” (extract) may serve as a good substitute for the fresh extract of meat particularly prepared. A teaspoonful of this preparation is diluted with one to two table- spoonfuls of cold, or, at the most, lukewarm, water; the yolk of one egg may also be added. Meat-extract Ice ( according to v. Ziemssen ). — One k. of fresh beef is cut into pieces the size of a hand, and is wrapped in coarse lattice-like linen, put under a lever-press and slowly pressed ; this is best done by an apothecary. The juice is caught in a porcelain dish. In this way one gets about 500 gm. This is mixed with 250 gm. of sugar and 20 gm. of freshly pressed lemon-juice (though this had better be omitted for dyspeptics), and 20 gm. of cognac, containing extract of vanilla, which has been well stirred with 26 o DIET LISTS. the yolks of three eggs, are added, and the whole is placed in a freezer. Bottled Bouillon ( accoi'ding to Uffelmanri ). — Three hundred gm. of fresh, lean meat are cut into small blocks and, without any ad- dition, are put into a clean bottle with wide mouth. This is closed, if there be no suitable stopper, with a stopper of pure, sterilized cotton, and placed in a vessel of warm water, slowly heated, and the water should be allowed to boil one-half hour. The bottle, which is now to be taken out, contains about ioo gm. of a turbid, brown broth, which is poured off without straining. Simple Bouillon, or Beef-tea. — One-half of a k. of lean beet is cut into small pieces, put into a pot holding about three liters, with a well-fitting cover, or into a steam cooking apparatus. This is to be filled with cold water, and the meat to be boiled three to four hours. According as the bouillon is desired concentrated or dilute, the liquid which evaporates must be replaced by the addi- tion of boiling water. Finally, one obtains about two liters of bouillon, and the meat which remains is of no further use. To obtain greater palatability and a prettier color the meat may be first browned in a little hot, pure lard before cooking, fresh soup herbs or a handful of dried Knorr’s julienne added; then finally add the three liters of cold water. Meat-jelly ( according to Hepfi ). — Good beef, free from fat and bones, is cooked on the water-bath with a little water for sixteen hours, until it congeals into jelly. Often one is compelled to use artificial preparations in the making of bouillon or in strengthen- ing weak bouillon. The most reliable in this respect is Liebig’s extract of meat (about ten c.c. to 250 gm.), or Cibil’s bouillon (one tablespoonful to 250 gm.); very convenient also are Quaglio’s bouillon capsules. If at the same time one wishes to give to the bouillon an increased nutritive value, one can add one teaspoonful of meat-peptone; or either Mosquera Julia beef-meal, Armour’s vigoral, or Valentine’s meat-juice may be used. A preparation which is often of service is Leube-Rosenthal’s meat solution. One k. of beef is chopped fine, put into a vessel with one liter of water and twenty gm. of pure hydrochloric acid, which vessel is put in a Papin steam cooking apparatus, in which it should boil ten to fifteen hours (with frequent stirring). After this the mass is put into a mortar and ground to an emulsion. After a further cooking of fifteen hours with bicarbonate of soda it becomes neutral, and is then steamed to a consistency of mush, PREPARATION OF SOUPS WITH FILLERS. 26l and put into four cans, which are to be soldered. As the making of this preparation requires much time and particular care, it is advisable to procure it from one of the following firms, who put it upon the market in cases of k. (enough for an adult for one day) : Armour & Co.,* Parke, Davis & Co.,f Dr. Mirus’sche Hof- apotheke (R. Stutz),J Huffner’s Hof- und Ratsapotheke (R. Wahr- burg),! C. Reinhardt (formerly Charrier).§ Soups with Fillers. (a) Soups with Fillers from the Cereal Kingdom . — The grains in question (such as barley or peeled barley, oats, green corn, rice) should be softened the night before in cold water, in which they are to remain until the following forenoon. Then the water is poured off and the grains are put on the fire with weak, cold bouillon, where they should be kept boiling at least three hours ; one-half hour before serving, the soup is strained through a fine hair sieve, and, after the addition of a little meat-extract, is made to boil again ; salt is then added as required, and to one plate of soup the yolk of one egg may be added. If one is to prepare a single plate of such soups, the soup meals of Knorr in Heilbronn are very serviceable, although they do not become gelatinous like the soups prepared from whole grains, and are not so appetizing. These meals must be stirred with cold bouillon to a thin liquid mass, and allowed to run into boiling beef-tea, which after that must boil at least one to two hours longer. Twenty gm. of meal is calculated for one plate of soup. In serving, one can add also the yolk of an egg. The nutritive value of these soups may be considerably increased by the addition of aleuronat flour. It is best to take eight gm. of aleuronat flour and sixteen gm. of oat- or green-corn meal for one plate of soup. || The aleuronat meal is mixed with cold water (or beef-tea), and is added to the soup only after the latter has boiled one-half hour. The meal swells hardly at all, and for that reason more of the two flours is to be taken than is necessary, ordinarily, in making of soup. Soups prepared with twenty gm. of oatmeal, or leguminose meal, barley-meal, tapioca, rice, etc., have a combustion value of about seventy to seventy-five calories, which is increased about sixty calories by the addition of the yolk of one egg. * Chicago. f Detroit, Mich. J Jena. g Berlin W., 27 Behren Strasse. || Can be procured from Dr. Hundhausen’s Starkefabrik, Hamm in Westfalen; 4^ k. cost seven marks, C. O. D. 262 DIET LISTS. ( b ) Tapioca Soup. — For this soup the French tapioca of N. & J. Bloch in Paris, and Knorr in Heilbronn, had best be used, which can be had in most of the larger fancy groceries in packages of 250 gm. For one plate of soup a heaped teaspoonful of these grains is boiled for half an hour with beef-tea, which has been boiling for some time previous, and to this, after a quarter of an hour, a little extract of meat, sufficient to cover the point of a knife, is added; if this be added later, just before serving, the taste of the extract is easily distinguished, which is disagreeable to many patients. (c) Sweetbread Soup. — The sweetbread is soaked for one hour in cold water, which is during this time often to be renewed ; then it is boiled in slightly salted beef-tea or salt water (to which one may add one teaspoonful of julienne for improving the flavor) for one hour. After it is cooked completely soft it is taken out of the beef-tea and freed from all skins, blood-vessels, etc. Now it can be cut either in pieces the size of a walnut, which one lays on the soup-plate and then pours over the beef-tea, or the sweetbread can be forced through a fine sieve ; beef-tea is poured over the mass and the whole is again put on the fire until it boils, after which the soup maybe served. The latter proceeding is rather to be recom- mended in the case of dyspeptics. One hundred gm. of sweet- bread (raw) is equivalent to about 90 calories. ( d ) Brain Soup. — A calf’s brain is allowed to lie in cold water for one hour, in order to draw out the blood contained in it ; then the water is poured off, the brain is once more thoroughly washed and cooked in weakly salted beef-tea or salt water, with the addi- tion of one teaspoonful of julienne, for one hour. Then immedi- ately force it through a fine sieve, dilute the mush with beef-tea, and cook it again. In serving, the yolk of an egg may be added. One hundred gm. of calf’s-brain equal 140 calories. (e) Soup Containing Meat ( according to Professor M. Rosenthal ). — Scraped raw beefsteak is chopped fine and forced through a sieve ; the mass, soft as butter, is thoroughly mixed with the yolk of an egg, and mixed in minute particles to a greater or less degree with boiling soup. (/) Meat- puree Soup ( according to Hedwig Heyl). — Twenty gm. of grated rolls are cooked for one-quarter of an hour with of a liter of bouillon. Stewed chicken-meat is pounded fine, passed through a hair sieve, and 25 gm. of it are stirred together with one tablespoonful of cream or one teaspoonful of meat-peptone ; PREPARATION OF SOUPS WITH FILLERS. 263 several spoonfuls of soup are added, and now beaten up with the entire mass, and served without further cooking. (g) Roll Soup (according to Hedwig Iieyl). — Thirty gm. of grated rolls are roasted with ten gm. of butter, without coloring the latter ; ^ of a liter of bouillon is poured over and slowly boiled for half an hour. The yolk of an egg is beaten up with a table- spoonful of sweet or sour cream, and then put into the soup, and the latter is passed through a sieve upon the previously warmed plate (equal to about 240 calories). (h) Soup Biscuit. — Forty gm. of butter are stirred for one- quarter of an hour, afterward mixed with two whole eggs, a little salt is added, and at last 40 gm. of flour. In order to make the mass rise more easily, one can add three gm. of baking-powder (consisting of bicarbonate of soda and tartaric acid, which can be had in most drug-stores in packages of 30 gm.). A long, square, sheet-iron mold is rubbed with butter ; the mass is put into it and baked in the oven with moderate heat for half an hour. When the biscuit has cooled off it is taken out, cut into blocks, and can then be added to the various soups (such as sweetbread, brain, or pea soup). The whole mass corresponds to about 630 calories. (i) Noodle Soup ( Vermicelli Soup). — The noodles (only the best quality) must be boiled half an hour in very good bouillon. A soup of about ten gm. of vermicelli equals about 50 calories. (P) Butter -dumpling Soup. — Thirty gm. of butter is stirred one- quarter of an hour, one whole egg and a little salt being added ; stir the same and mix well with the butter, and then add 30 gm. of flour. With a teaspoon rather long lumps are cut out of the dough and put into boiling beef-tea, in which they must boil twenty minutes more on a fire not too strong. The whole mass equals about 420 calories. (/) Green-pea Soup (Mashed). — Fresh green peas are boiled in salt water until thoroughly soft ; in advanced seasons, when they are no longer very young, add ^ of a gm. of carbonate of soda ; canned peas are also very good at any time for making this soup. Let the water run off through a strainer, force the peas through a fine sieve, mix with a teaspoonful of flour (aleuronat flour), pour beef-tea over the mass and cook again; 100 gm. of peas equal 75 calories ; of a liter (420 gm.) of peas gives 280 gm. of mashed, equal to 300 calories. DIET LISTS. 264 II. Fish. Fish for the table of a sick person should never be boiled or fried in fat, but boiled only in water. Of the fresh-water fish the trout, the perch-pike ( Lucioperca sandra), pike, carp, grayling, and salmon come under consideration here. Of salt-water fish the black or sea-bass, sea-trout, the bluefish (. Pomatomus saltator ), the mackerel, cod, rockfish, and haddock are suitable. The fish is carefully freed from scales, rubbed inside with salt, and boiled in very strongly salted water, in which it is allowed to remain, accord- ing to its size, from one-quarter to one-half hour. All spices are to be omitted; only a handful of dried julienne may be put in the boiling water, by which the flavor is considerably increased. All fat and pungent sauces are to be avoided, and even hot butter will generally not agree with the dyspeptic ; so that it is best to put only a little fresh butter on the fish when serving. Of the sea- fish, the cod, rose-fish, and haddock are to be recommended. Their preparation is the same, except that they are soaked one-quarter of an hour previously in fresh water (not in boiling, but cold water), in which is put a large quantity of salt and also some julienne. The vessel must be large enough to allow the fish to be surrounded on all sides by the water. A two- or three-pound haddock must remain on the fire thirty to forty minutes to be thoroughly done ; sea-fish also are to be served with fresh butter. III. Meats. 1. Sirloin (Fillet ). — For the tenderness of beef it is of impor- tance that it be allowed to hang long enough ; for this two to four days are necessary in summer, in winter as many as eight days ; only in the coldest season must it be protected from frost, through which it becomes very dry. The meat is freed from all fat, the membranous parts, well beaten, washed and salted, and then put into a stewpan with hot lard, in which it is quickly turned over several times. The meat loses, in roasting in the English style, ten per cent, in weight, and in slow roasting, thirty per cent, in weight. To prepare a fillet in English style, so that it is still red inside, one calculates for each pound of meat one-quarter of an hour; so that a four-pound roast requires one hour’s roasting. It is entirely unsuitable to try, by means of sticking with a fork, how far the roast is done, for much juice is lost by this, and the cook must learn by practice, by the nature of the pan, the thickness of the roast, the strength of the fire, to calculate the period of time neces- PREPARATION OF MEATS. 265 sary for the completion of the roast. During roasting frequently add spoonfuls of beef-tea, so that the butter does not become too dark, but the bouillon must never be poured upon the meat itself. One-quarter of an hour before serving, the roast is taken out of the pan, all fat is carefully skimmed from the sauce, a tablespoonful of white flour and a teaspoonful of aleuronat flour are mixed with a little cold bouillon, a little extract of meat is added, and this thin mixture is then added to the sauce of the roast, which is again made to boil, and the roast is again laid into it until serving. One hundred gm. of beef roasted in English style equal about 210 calories. 2. Roast Beef. — This roast is good and juicy only when in large, thick pieces. The preparation is exactly the same as the preceding. It is juicier when roasted on the spit, though in most households the necessary equipments are wanting. With this meat, which has a tolerably coarse grain, a sufficient time for hanging is absolutely necessary. 3. Raw Beefsteak ( according to Lenbe). — From the loin, which has hung a sufficient time, as much meat is scraped off with a dull spoon-handle as can be separated without violence, until one has a mass of about 150 gm. The mass thus scraped off is slightly salted, made into a very small cake, and eaten either entirely raw or just roasted on the surface in fresh butter. One hundred gm. equal about 120 calories. 4. Beefsteak ( according to Wiet). — Take some of the best sirloin and cut across a piece as thick as a thumb ; after this has been well pounded and slightly salted on one side, it is put into an iron or enameled pan, fried for one minute on one side in fresh butter, then turned, gravy poured over, and is fried on the other side only one-half of a minute, after which it is immediately served on a warmed plate. One hundred gm. equal about 130 calories. 5. Beefsteak in Oil. — From a well-hung fillet a piece as thick as a thumb is cut, all skins and fat removed, the same well pounded and salted. Then spread on both sides with the finest olive oil, cover up well, and allow it to remain thus two hours. Thereafter put into the pan and fry without any further grease (except the oil previously spread over it) till it is brown on both sides. The time necessary for frying varies from five to ten minutes, according to the degree one wishes it done inside. 6. Roast Veal . — The leg of veal, after it has hung a sufficient time, is freed from the thick outside skin and laid in sweet milk for 18 266 DIET LISTS. one or two days in summer, two or four days in winter, by which it becomes tender and soft. Before using, it is carefully washed, thoroughly skinned, and well salted ; thereupon it is larded with fresh lard and roasted in tolerably hot butter or white beef-fat, of which about 200 gm. are necessary. For the rest it is treated like any other roast, except that it is best (in the case of veal) to roast until well done, which for a small roast takes two hours, for a large one three hours. In the English way one and one-quarter to two hours are sufficient. Roast veal, when the bone is not pre- viously taken out, gives a very good, thick sauce"; so that in most cases it is necessary to add only a little bouillon after the fat has been skimmed off. Its value in calories is about the same as that of lean beef. 7. Veal fricandeau is also laid in milk a few days before using, which milk it is best to let sour, for the flavor is thus increased; it must be done, however, in such a manner that the milk covers the meat completely. For the rest, the meat is treated as any other veal roast, except that one and a half hours’ roasting with a good fire will suffice. The sauce is to be mixed with flour, and it can be given a piquant flavor by the addition of some cream. 8. Veal Cutlets {Chops ). — The ribs of the calf are separated from the backbone ; the single cutlets separated from each other are washed and freed from skins, pounded, salted, and fried in a pan with hot butter. They will be more tender if they have lain one day previously in milk; in this case they need be fried only eight or ten minutes, but otherwise it is preferable to fry them from one- half to one hour, not leaving them long in one place, often shoving them to and fro, during which time a piece of fresh butter is also added, and the melted butter is constantly poured over the cutlets. Before serving, some good liquor from a roast is added. To cover cutlets with bread-crumbs is not advisable in dietetic cooking. One hundred gm. of fried veal cutlets (also the following veal dishes) equal 230 calories. 9. Scotched Collop . — From the leg of veal,, which has lain in milk two or three days, cut slices as thick as your thumb, wash, beat and salt them, and put them in a pan with hot butter, where they must be allowed to brown slightly on both sides. Then pour in one glass of white wine and some bouillon, cover up tightly, and let them steam altogether for about one and a quarter hours, pouring in some bouillon from time to time. The addition of sour cream improves the flavor ; but the digestibility is decreased by PREPARATION OF FOWL, POULTRY, ETC. 26? the sour cream. Then skim off all fat and with Hour prepare a sauce as directed above. 10. Fillet of Veal . — From the fricandeau piece cut strips one cm. thick and six cm. wide, and prepare them exactly as in No. 9; in the middle lay a few pieces of middling, roll them up and tie with cord. For the rest proceed exactly as in the case of scotched collop. 1 1. Veal Steak . — Cut from the leg pieces as thick as your thumb, weighing about 100 gm., pound them well, wash, salt and lay them in a pan with hot butter, and fry them, with frequent turning, for ten minutes. Either add some sauce from a roast or prepare one from bouillon, flour, and meat-extract, which is put into the pan, and then let the steaks fry in it for two minutes longer. 12. Lamb's Saddle . — The saddle of a young animal is laid in milk for two days, or the milk is allowed to sour, through which a venison-like flavor is obtained. Before using, the roast is washed, freed from fat and skins, and larded with fresh, unsmoked bacon; then it is put into a pan with previously heated beef-fat or good butter, in which it must immediately be turned several times. It is roasted one and a half hours, during which time it is to be dili- gently basted by the addition of beef-tea. In the last hour pour in one glass of white wine and as much bouillon as the sauce has boiled down. With sour cream the roast becomes particularly well flavored, but not every patient can stand it. The sauce is pre- pared, as in other roasts, with flour. 13. Roast Fowl . — Fowl destined for roasting must be picked and cleaned immediately after killing, and then it is allowed to hang in a cool place at least one day ; in winter, two to four days — for which reason one should always inquire, in buying dressed poultry, how long it has been killed. (a) Young cockerels must be scalded before picking. Before roasting, the hair must be singed off, and they must be carefully washed and rubbed with salt inside and outside ; afterward they are put in a pot with plenty of hot butter, roasted brown on both sides, with frequent basting, for which three-quarters to one hour is necessary. The sauce is made as above, with a little flour. One hundred gm. of raw chicken equal 100 calories. ( b ) Capons and pullets should be roasted with little butter, since they are generally fat enough. According to their size they must be roasted, with frequent basting, from one and one-half to two hours. 268 DIET LISTS. (c) Young pigeons are treated just as young cockerels. Time of roasting, about three-quarters of an hour. ( d ) The pheasant yields a fine roast after it has hung about eight to fourteen days. Roast it from two to three hours, with plenty of butter and frequent basting. ( e ) The Partridge. — The same must be young, and must have been killed several days before using, in order to furnish a tender roast. After it has been picked, cleaned, and washed, it is put into a tolerable quantity of hot butter, and a piece of fresh butter is also put inside the partridge. On the other hand, wrapping with bacon is less to be recommended for those having stomach trouble, and a roast just as juicy can be obtained by diligent basting; the palatability can also be increased by the addition of white wine and sour cream. Time of roasting, one and one-quarter hours. (/) Boiled Cockerels and Pigeons. — They are prepared just as for roasting, then laid in boiling, slightly salted bouillon, to which a little julienne has been added, and boil one to one and one- quarter hours. Very young pigeons are cooked soft in three- quarters of an hour; likewise very young cockerels. 14. Roast Game. {a) Roast Hare. — The hare is skinned and then cleaned, but the liver, heart, head, etc., are not to be used in cooking for the sick. After the roast has been thoroughly washed within and without, it is well salted and larded with fresh (not smoked) bacon, and treated exactly as the roast lamb, so that it is done in about one and one-half hours. By the addition of sour cream the roast hare becomes very good, but in this way it does not agree with every one. The sauce is prepared in the same way as in the case of fillet roast, with flour and beef-tea. ( b ) Roast Venison (Doe). — The venison saddle is the most bene- ficial game for those who have stomach troubles. It is to be treated exactly as the roast hare, only it must be roasted about two and one-half hours, on account of its size. The joint of venison will gain considerably in tenderness and flavor if it is laid in light red wine a few days before using; for the rest it is to be treated exactly as the venison saddle, only it must be roasted two and one-half, three, or four hours, according to size. The sauce is the same as with roast hare. But game can also be treated in the English fashion, by roasting it only a short time, as in the case of fillet and roast beef. A venison joint thus requires one and one-quarter hours, approximately, with strong heat, and, if very heavy, one and STEWED MEATS. 269 one-half hours. A venison saddle, if young and tender, requires three-quarters of an hour; if older, one and one-quarter hours. In this way the meat remains juicier and stronger. (< c ) Venison saddle (stag) is to be treated in the same way, except that it must be roasted a correspondingly longer time ; but generally the meat is not as tender and palatable as that of the doe. One hundred gm. of game (roast) equal about 215 calories (when thoroughly done). 15. Stewed Meats. (a) Preserved Veal. — The meat from a leg or breast which has hung sufficiently is cut into pieces the size of a walnut; the latter are put into a small stewpan with hot butter, and a little salt sprinkled over ; immediately after they have been once turned in the butter, y 2 of a glass of white wine, about 75 gm., is poured in and the whole covered up well and stewed for one and a quarter hours with moderate heat, some good bouillon being added from time to time. One-quarter of an hour before serving, the sauce is prepared in the way before indicated ; and immediately before serv- ing, the yolk of an egg is mixed with water and put into the sauce. ( b ) Preserved Sweetbread. — The sweetbread is cooked till it is soft as in the case of soup, is skimmed, cut into two halves, and ten minutes before serving is laid in butter-sauce, to be prepared in the following way : A little piece of butter is melted in a small dish, without being allowed to brown ; then one tablespoonful of flour is added, well mixed with the butter; then pour in cold bouillon and a little white wine, so that, after the sauce has boiled, the whole forms a tolerably thick liquid. The amount of the ingredients must be determined by the amount of sauce desired. Before serving, the yolk of an egg is added to the sauce. (e) Stewed Cockerels or Pigeons. — A young cockerel or pigeon is dressed as for roasting, quartered into equal parts, slightly salted and laid in a stewpan in which a small piece of butter has been pre- viously melted without being browned. The stewpan is covered tightly and the poultry stewed slowly for a quarter of an hour. Then y of a glass of white wine, about 75 gm., and some good bouillon are added, and it is again allowed to stew for about three- quarters of an hour longer, a little beef-tea being added from time to time. The sauce is the same as in the case of stewed veal. One hundred gm. of meat equal about 120 calories. 1 6/ Dishes from Chopped Fresh Meat . — Be warned against allow- ing the butcher to chop the meat, as in some cases less desirable or 270 DIET LISTS. less appetizing meat may be mixed in. Every household should possess a machine for chopping meats ; in cases where there is none, do not mind the trouble of chopping or, preferably, scraping it yourself. (a) Roast Chopped Meat. — One-half of a pound of veal, y 2 of a pound of beef, and y 2 of a pound of pork, not entirely lean, are put through the chopping machine; the whole mass is then mixed in a dish with three whole eggs, y of a liter of milk, I y grated rolls, and a tolerable amount of salt ; if the dough then seems too stiff, a little more milk may be added. The mass is made into a longish cake and roasted in hot lard or good butter (ioo gm.) first on one side and then on the other, until it is light brown. Time, one hour and a quarter. From this hardly any sauce will be obtained ; hence one must be prepared from flour, bouillon, extract of meat, and a little white wine, which is to be poured over a quarter of an hour before serving. One hundred gm. of this roast equal about 250 calories. ( b ) Cutlets from Chopped Meat. — The same mixture as in the preceding is made into little cutlets, allowed to fry on both sides in hot butter until light brown ; then skim off all fat, prepare a butter sauce, pour it over, and let it fry with this for another half-hour. ( c ) Meat Balls (Veal). — One pound of meat from the leg is chopped up fine in the machine ; 40 gm. of butter are stirred to foam, two whole eggs, and one roll, grated fine, are added ; also a little salt, and according to taste of the individual a little finely chopped parsley. Of this mass flat cakes are made and cooked for one-quarter of an hour in salt water ; butter sauce, or, when allowed, anchovy sauce, is added, which is to be poured over the cakes one-quarter of an hour before serving. One hundred gm. equal 250 calories. 1 7. Dishes from Chopped Roast Meat. (a) Hash. — In a little butter or lard put some finely chopped roast meat (veal, fowl, or game), stew for five minutes with frequent stirring and pour over any sauce remaining from the roast, or make a special sauce as follows : Sprinkle some fine flour upon the stewed meat, mix well, pour in a little white wine and enough bouillon so as to produce a rather thick gruel. Then stew for one- quarter of an hour longer with moderate heat, keeping the vessel well covered. The hash is now done. A little extract of meat added will improve the flavor. One hundred gm. equal about 225 calories. PREPARATION OF JELLIES. 27 (, b ) Meat Pudding. — Sixty gm. of butter are stirred until foamy, four yolks of eggs, salt, and a little fine-cut parsley added. Two French rolls are grated fine, the inside cut into small pieces and soaked in milk, in which it remains one hour; 170 gm. of roast meat are cut fine or chopped in a machine ; the grated rolls are taken out of the milk, pressed, and with the chopped roast meat mixed with the other mass (butter and eggs). If allowed, two tablespoonfuls of sour cream may also be added. Lastly, the whipped whites of four eggs are mixed in, and the whole dough is put in a mold rubbed with butter and stewed with dust from the rolls. In this the pudding is cooked for one and three-quarter hours in a water-bath. Any sauce remaining from a roast is added (or anchovy sauce). One hundred gm. equal about 200 calories. (c) Omelette Souffle from Remnants of Roasts. — Forty gm. of finely cut roast meat are mixed with one tablespoonful of sweet or sour cream ; a little salt and the yolk of an egg are added ; the whipped white of an egg is mixed in ; the mass is put into a small porcelain mold and baked in a well-heated oven for twenty min- utes ; sauce from a roast is added. The whole mass equals 215 calories. (< d ) Sweetbread Pudding (according to Hedwig Hehl). — Twenty- five gm. of French rolls are grated and laid in milk. The sweet- bread is cooked, until soft, in bouillon or salt water, skinned, and cut into small blocks. Thirty gm. of butter are stirred until foamy, and two yolks of eggs, the roll which has been pressed out, a little salt, parsley, and the blocks of sweetbreads are put into the butter, with which the whipped white of an egg is mixed ; the whole is put into a cup' well rubbed with butter, covered, and cooked for three-quarters of an hour in the water-bath. Anchovy sauce or meat gravy is added. One hundred gm. equal about 150 calories. IV. Jellies. 1. WieVs Jelly , for Dyspeptics . — Takeoff the skin and meat from a calf’s foot, mash the bones, and put on the stove with some cold water until it is heated to foaming, when all refuse will be sepa- rated. After rinsing off the scum with cold water, put the bones with y of a k. of beef, or y 2 of an old hen, and 1^ liters of water, and five gm. of salt, and boil slowly from four to five hours. Pour the jelly thus formed through a fine sieve, and place overnight in the cellar. Next morning take off the layer of fat, and to clarify the cold jelly add one egg with the mashed shell, and mix with steady 272 DIET LISTS. beating and stirring. Then subject the whole with constant beating and stirring to a temperature of not over 6o° R. (or else the white of the egg will curdle). If the jelly begins to show grains, cover and let cool until the white of egg becomes flaky and separates. Hereupon strain a few times more until it becomes perfectly clear, add five gm. of extract of meat, and pour the jelly into a mold and let cool again. An addition of gravy from a roast is very pala- table. It must be mixed in while the mass is still warm and liquid. The dish is very palatable with cold fowl, but does not keep well in summer, and had, therefore, best be put on ice. 2. Ichthyocolla Jelly . — Cut fifteen gm. of ichthyocolla into small pieces and let soften in ^ of a liter of cold water for eight to ten hours ; boil for one-quarter of an hour and add gravy from a roast and extract of meat. Pour the mass when hot through a fine cloth, or, better, through filter-paper. One can add to 100 gm. of the liquid also 0.5 gm. of hydrochloric acid or ten gm. of white wine. 3. Milk Jelly . — Boil two liters of milk for five to ten minutes with 250 g nl * of sugar. To the well-cooled mixture add, while slowly stirring, a solution of thirty gm. of white gelatin in 250 gm. of water, and also add three wineglassfuls (400 gm.) of good Rhine wine, or thirty gm. of cognac ; afterward pour the mass into a form and let cool. One hundred gm. equal about 250 calories. V. Vegetables. 1. Asparagus . — The asparagus stems are washed, peeled from the top downward, and the lower woody ends cut off ; then they are bound in a small bundle, and cooked until soft in salt water, which requires, according to the thickness of the stems, one-half to one hour; a large quantity of water must be used in cooking, otherwise the asparagus easily takes an ugly color. Make a butter sauce with yolk of egg. Dyspeptics can take only the soft heads without sauce. One hundred gm. equal about 20 calories. 2. Spinach . — The spinach leaves are carefully picked, washed, and laid in boiling salt water, in which they are to be cooked slowly, without being covered ; otherwise they lose their color easily. After twenty minutes put them on a sieve, pour cold water over them, and press them. Then cut the spinach very fine or pass through a hair sieve, lay in a little melted butter, dust flour over it several times, and add strong bouillon. Lastly, mix in the yolk of an egg with cold bouillon. One hundred gm. equal 165 calories (prepared from 250 gm. of spinach leaves). PREPARATION OF VEGETABLES. 273 3. Comfrey or Brnisezvort. — Wash, clean carefully, cut in pieces two inches long, and also split the thicker pieces lengthwise. Mix one tablespoonful of flour with one liter of water and one table- spoonful of vinegar, and lay each cleaned piece of root in the mix- ture. Afterward they are again rinsed on a sieve with clean water, laid in melted butter, salted, covered tightly and stewed, adding strong bouillon from time to time. According to size and age the roots require boiling from three-quarters to one and one-half hours in order to become soft. One hundred gm. equal about 1 20 calories. 4. Green Peas. — The peas (j^) are hulled and stewed in 15 gm. of butter and bouillon as the preceding; time, from one to one and a half hours. Or, take canned peas and put the opened can in hot water, or cook them with the same amount of butter and some salt. For the sick it is advisable to pass the peas through a sieve and serve them as a puree. One-half of a liter of peas yield 280 gm. of pea puree; of this* 100 gm. equal 160 calories. 5. Carrots. — Carrots are serviceable in the dietetic kitchen only when very young and tender. They are cleaned, washed, cut into pieces and then stewed similarly to peas. The time is also the same. If it is desired to serve them as a puree, they are passed through a hair sieve after they are cooked. A little flour is dusted over them and they are cooked to a thick mush. One hundred gm. of puree equal 120 calories. 6. Beans [Green). — Young beans are cleaned, washed, cut fine, and, like the peas, stewed in butter and bouillon. In a season when there are no young, fresh vegetables, one can use to advan- tage canned beans, of which Prince beans (Flagiolettes) are the most tender. One hundred gm. equal about 40 calories. 7. Cauliflozver. — The cauliflower is cleaned, washed, and treated like the asparagus. Time of cooking, one-half hour. One hun- dred gm. equal about 60 calories. 8. Rice in Bouillon. — Thirty gm. of rice are washed twice on the previous evening, and then water in which a little carbonate of soda has been dissolved is poured over it, so that the rice may swell during the night; then the water is drained off, and the rice with a piece of butter and some strong bouillon is put in a stew- pan and stewed for one and one-quarter hours, tightly covered, except the last quarter of an hour; finally the beaten-up yolk of an egg is added. Now rinse out a small porcelain dish with cold water, without drying it, and press the rice into it, let stand five minutes and then turn the mold. The amount is calculated for one 274 DIETETIC KITCHEN. person, and is best suited for a side dish to meats. The whole equals about 225 calories. 9. Chestnut Puree. — One-half kilo of chestnuts are peeled and boiled in water so long as to get the second (inside) skin off easily. The chestnuts are laid upon a sieve until all the water has drained off. Then they are mashed in a dish and afterward pressed through a hair sieve. One hundred gm. of butter are melted in a stewpan on the fire; a little salt and sugar, enough to cover the point of a knife, are added (to the butter), and then the chestnuts are put in. Stew them, with frequent stirring, for one-half hour, and pour in enough bouillon to get a mush not too thick. VI. Side Dishes From Eggs and Flour. 1. Scrambled Eggs . — Two eggs are thoroughly beaten with a little salt until the yolk and white are completely mixed. Then melt five gm. of butter in a small enameled vessel, add the egg mixture, and heat, with continued stirring, until a rather thick mush is formed. Serve in a well-warmed dish. This dish is suitable with cold roast, ham, smoked meat, etc. Two scrambled eggs equal about 200 calories. 2. Potato Puree . — Peel ^ of a pound of very mealy potatoes, cut into quarters, wash, and cook until soft in a steam-cooking apparatus; then pass through a coarse hair sieve; add 20 gm. of fresh butter, a little salt, and 60 to 70 gm. of warm milk, and beat thoroughly for five minutes while the mixture is on the fire, until it becomes very foamy. This must only be prepared just before serving, as it loses flavor in standing. One hundred gm. equal about 125 calories. 3. Suabian Dumplings . — One hundred gm. of flour, two eggs, two tablespoonfuls of milk, and a little salt are thoroughly stirred together; the dough is put in a special sieve (coarse), through which it is forced and allowed to drop into strongly salted boiling water. One must take a large pot with plenty of water, so that the dumplings may rise better ; they are allowed to boil for half an hour. When done they are poured on a large sieve, and remain until all the water has drained off. Meanwhile melt in a stewpan ten gm. of fresh butter, put the dumplings into it, shake them well, and serve. The sieve necessary is known only in South Germany, but it can be made by any tinner, for it is like an ordinary strainer, the holes having a diameter of one cm. (about J- of an inch). One hundred gm. equal 175 calories.. EGG AND FLOUR SIDE DISHES. 275 4. Roll Dumplings . — Rolls from the day before are grated (that is, the crust), the inside is cut into slices and cold milk poured over until the bread is thoroughly soft, for which at least an hour is necessary. Meanwhile stir 60 gm. of butter for one-quarter of an hour, and add slowly four eggs and a little salt. Then squeeze the milk out of the slices and stir them with the butter and eggs until finely divided. In order to test whether the mass be of the right con- sistency, make a lump as large as a walnut and boil in salt water. If it breaks, a little dust from grated rolls must be added. When the dough has acquired the necessary firmness, make dumplings the size of an apple (about seven from the given quantity of ingredients). After they have boiled well for one-quarter of an hour in salt water, take them out with a sieve spoon, cut in half, and serve. One hundred gm. equal 250 calories. 5. Vermicelli ( Water Noodles or Vegetable Noodles '). — For the dough take 180 gm. of flour, and three eggs, which are to be mixed with the flour in a dish ; then put the dough on a board, and knead well with the hands until it is tender. Then form it in the shape of a long sausage and cut into four equal parts. First take one part : knead into a flat, round cake ; weigh off, in addition, 20 gm. of flour ; dust the board and rolling-pin with this, and roll out thin (20 gm. of flour will suffice for all the four parts of the dough). At each turning of the dough dust the board again with flour, so that the dough may not stick and tear. The necessary thinness is reached when one can distinguish through the dough the pattern of a piece of calico, etc., laid underneath. When thin, lay the four parts on a clean, white cloth near the fire; let them become half dry, and cut into strips one cm. broad, which are to be separated and hung up in the kitchen for twelve hours to dry. They can be kept for some time in a tureen. When using, lay them for ten minutes in boiling salt water; pour off the water through a strainer, and put the noodles in a dish. Vegetable noodles of a very good quality are now also made by factories. One hundred gm. of boiled noodles equal about 190 calories. 6. Macaroni . — Buy only the best quality. Put in a vessel with much boiling water, and after it has boiled ten minutes pour off the water; pour over some more boiling salt water and let boil for half an hour. Drain, put in astewpan with a little butter (which is on the fire), mix, and serve immediately. One hundred gm. equal about 150 calories. One can also, instead of putting hot butter over the macaroni, add a butter sauce, described under 2/6 DIETETIC KITCHEN. “preserved sweetbread.” When the macaroni has been drained, put in a porcelain dish in which it is served, pour the thickish sauce over and put the dish for ten minutes in the oven. VII. Flour, Milk, and Egg Dishes. 1. Rice Mush . — Thirty gm. of rice (Caroline rice is the best) are twice thoroughly washed the night before ; then cold water, in which a little carbonate of soda has been dissolved, is poured over, and allowed to stand until the next day. Before using, the water is poured off ; of a liter of milk is boiled and the rice then added and boiled, well covered up, for one and one-quarter hours on a moderate fire, with frequent shaking. If the milk becomes too thick from boiling before the rice has been thoroughly softened, add a little more hot milk. Whip the whites of two eggs, and just before serving mix lightly with the rice; if it is desired to make it more nourishing, the yolks of the two eggs can also be added before the whites (this quantity, for one person, equals 700 calories). One hundred gm. equal about 160 calories. 2. Tapioca . — Boil of a liter of milk ; mix 20 gm. of best im- ported tapioca and boil for one-quarter of an hour longer, with constant stirring. Further procedure same as with rice (in the same way oatmeal may also be treated). Value in calories of above quantity, about 250. 3. White Pot . — Moisten in a small, well-enameled pan 65 gm. ot fine sugar with one tablespoonful of water, and burn to caramel sugar. This requires great care, for the sugar easily becomes too dark and then takes on a bitter taste. On a hot stove, not over an open fire, one must constantly stir the sugar with a tin spoon until it gets a fine brown color. During this process heat a tin form, such as are usually used for sweet dishes, jelly, etc., and pour into it the sugar as soon as it has browned, and let it spread on all sides until the surface of the plate is covered. Then let cool. Now beat up three whole eggs in a dish, add of a liter of unboiled milk, the contents of a package of vanilla, or of a stick of vanilla boiled in milk, powdered sugar to taste, mix the whole thoroughly, and pour into the form with the sugar, which is now cold. Put on a water-bath, cover, and boil until the mass has amalgamated, which can be tried by thrusting in a teaspoon. Take out the form, allow it to cool, and turn over on a plate. This is a pleasant, cooling, well-tasting dish, nourishing as well as easily digestible. One hundred gm. equal about 30 calories. PREPARATION OF PUDDINGS. 2 77 4 * Egg Creme ( according to Mrs. Dr. Pariser). — For this one reckons, for one person, one yolk of egg, two tablespoonfuls of beaten cream flavored with vanilla, sugar according to taste, and a few drops of arrack or cognac. The yolk of egg is first beaten with sugar to foam. Then the whipped cream is added and well mixed in ; lastly, a few drops of arrack or cognac are added, and the whole served in wineglasses. 5. Vanilla Creme {according to Mrs. Dr. Hughes'). — Stir four yolks of eggs to foam, with of a pound of fine sugar ; boil of a liter of milk 'with some vanilla and add immediately to the eggs ; mix with an egg-beater and again put on the fire, with continual stirring. Six pieces of white gelatin are dissolved in a little hot water and poured into the mass while the latter is still on the fire. As soon as it is risen, take quickly from the fire, pour through a strainer and nearly allow it to cool, with constant stirring. Then the whipped whites of four eggs are added and the mass poured into a porcelain dish which has been rinsed with cold water ; allow it to cool, and turn over just before using. A fruit sauce may be served with the creme . 6. Roll Pudding. — Stir thirty gm. of butter until foamy, add yolks of two eggs, with one tablespoonful of fine sugar, fifteen gm. of grapes, fifteen gm. of raisins, and twenty gm. of finely grated almonds. The outsides of two French rolls are grated off, the insides cut in pieces, soaked one hour in milk, and then squeezed thoroughly and mixed with the rest of the mass. Now the whole is thoroughly mixed, the whipped whites of two eggs stirred in, and the dough put into a form rubbed with butter and dusted with roll dust. Either bake the pudding for three-quarters of an hour in the water-bath or bake in a small porcelain dish for one-half of an hour in an oven. Add vanilla or wine sauce. If necessary, the almonds, raisins, and grapes may be omitted. One hundred gm. equal about 250 calories. 7. Tapioca Pudding. — Thirty-five gm. of tapioca are cooked for five to seven minutes with of a liter of milk until it turns to a thick mush. Meanwhile stir to foam twenty-five gm. of butter ; add yolks of two eggs and one small tablespoonful of fine sugar, and stir this mass into the no longer hot, but still warm, mush. After rubbing a small porcelain form with butter, whip the whites of two eggs, add, and mix with the mass. Put into the form and bake the pudding in a well-heated oven for three-quarters of an hour. One hundred gm. equal 175 calories. 2 7 8 DIETETIC KITCHEN. 8. Flour-mush Pudding . — Melt twenty gm. of butter in a sauce- pan ; mix in smoothly fifty gm. of flour and of a liter of milk, and cook the mush until it separates from the pan. Then let cool a little, and add afterward one yolk of egg. Now stir until foamy twenty gm. of butter, to which add yolks of two eggs, I ]/ 2 tablespoonfuls of sugar and one teaspoonful of arrack, and with this mass mix the cooked mush ; then whip the whites of the three eggs, mix lightly with the mass, fill into a form rubbed with butter and dusted with roll dust, and let cook for one hour in the water-bath. One hun- dred gm. equal about 220 calories. 9. Rice Pudding. — Thirty-five gm. *of finest rice is soaked the night before, as in the case of rice mush. Heat ^ of a liter of milk, add the rice ; cover and cook slowly until entirely soft; stir 25 gm. of butter to foam, add two yolks of eggs and one tablespoonful of sugar. When the rice has become lukewarm, mix in the other mass ; whip two whites of eggs, put the dough in a porcelain form rubbed with butter, and bake in an oven for half an hour. One hundred gm. equal about 150 calories. 10. Biscuit Pudding. — Five yolks of eggs are stirred for half an hour with of a pound of fine sugar ; then add a small table- spoonful of fine flour and a little vanilla; also a little arrack and five whipped whites of eggs. Rub a pudding form with butter and dust with fine roll crumbs; fill in the mass and cook for one hour in the water-bath. One hundred gm. equal 215 calories. 1 1. Noodle Pudding. — Of the best egg noodles (fine) take seventy gm., crumble to pieces, throw into of a liter of boiling milk, and boil for half an hour. Meanwhile stir 50 gm. of butter until foamy, add three yolks of eggs and about one tablespoonful of fine sugar, and mix this mass with the half-cooled mush. At last whip the whites of three eggs, mix with the rest, put the whole in a form rubbed with butter, and bake the pudding for one hour in the oven. 12. Omelette Souffle. — Stir the yolk of an egg, with one table- spoonful of fine sugar, for a quarter of an hour; add on the point of a knife a little of the finest flour, one tablespoonful of arrack, and the whipped whites of eggs. In an omelette pan, melt five gm. of butter, and meanwhile put on the hearth a porcelain soup plate, which must fit the pan exactly, and heat the plate well. Then put the dough in the pan and cover this immediately with the hot plate. Now bake the omelette with a moderate fire until the surface has become solid, which requires four or five minutes ; then turn over on another warmed flat plate ; then fold in the middle, MISCELLANEOUS PREPARATIONS. 279 strew sugar over, and serve at once. The whole, about 240 calo- ries. 13. Souffle Baked in the Oven. — Stir the yolks of two eggs, with 35 g m - of sugar, for a quarter of an hour; add on the point of a knife a little fine flour, and one tablespoonful of arrack and the whipped whites of two eggs; then at once fill the dough into a porcelain form rubbed with butter, and bake for eight to ten minutes in the oven. The whole, about 370 calories. 14. Snowballs in Vanilla Creme. — One liter of milk, with one tablespoonful of fine sugar, mixed, is used in the cooking. The whites of four eggs, with one tablespoonful of sugar, are whipped until stiff. Then from the whipped eggs longish lumps are cut out with a tin spoon and these put into the boiling milk. The milk must be put on the fire in a largo, wide can so that the snowballs may expand. One must never put more than six in the pan at one time. When they have lain one minute in the milk, turn them ; let them lie another minute on the other side, take them out care- fully, and lay on a large platter. After the whole has thus been treated, take the four yolks of eggs, mix with a teaspoonful of fine flour, y of a liter of milk, and a package of vanilla, and make of them a creme. When this begins to boil take it from the fire; let it cool, and just before serving place the snowballs upon the creme in a porcelain dish. VIII. Miscellaneous. 1. Stewed Apples. — Peel good apples, cut them and stew with a little water and sugar, according to taste ; then pass through a coarse hair sieve. One hundred gm. equal about seventy-five calories. 2. Pears. — Peel good pears, cut in halves, but do not take out seeds, put on the fire with plenty of water and a little sugar, and boil until soft; a little wine added will improve the palatability. 3. Wine Sauce or Chandeau. — Two yolks of eggs are beaten up in a small pan with y 2 of a teaspoonful of the finest potato flour; then slowly stir in y of a liter of good wine and add two to three tablespoonfuls of fine sugar. Put on the fire and stir until the sauce has gained a thick consistency ; then immediately take from the fire and cover; now whip two whites of eggs, and pour the sauce into this slowly, with vigorous stirring, and serve at once. Reckoning the value in calories of the alcohol, 100 gm. equal about 1 10 calories. 28 o DIETETIC KITCHEN. 4. Vanilla Sauce . — Mix two yolks of eggs with one table- spoonful of fine sugar, add ^ of a liter of cold milk, a little vanilla or ]/ 2 of a package of vanillin. The sauce is put on the fire and stirred until it begins to thicken. Then take from the fire imme- diately and serve. One hundred gm. equal about 125 calories. 5. Aleuronat Bread ( according to Dr. Huth , “ Aerztl. Centralbl.,” August, 1894, No. 46). — Mix 500 gm. of aleuronat flour and 1500 gm. of rye flour; mix one-half of this mass with one liter of warm water, two good tablespoonfuls of salt, and 180 gm. of yeast finely divided in a little water ; set this dough, sprinkled with a little flour, to rise. After the usual rise the dough is worked up with the remaining flour into two loaves. These are baked in square pans (10, 15, 20 cm.) rubbed with butter; after letting them rise well once more, they are baked for two hours with strong heat. 6. Nutritive Enematci : (a) Meat Pancreas Clyster (according to Leube).- — One hundred and fifty gm. of good beef are scraped and then chopped fine ; 50 gm. of fresh pancreatic gland, free from fat (either of a cow or of a hog), are mixed with this and stirred carefully, wdth the addition of not more than 150 gm. of lukewarm water. Injections of from 50 to not more than 100 gm. at a time, in a lukewarm state, by means of a simple funnel, ending in a nozzle which must have a wide opening. The mixture will keep only a short while. One hundred gm. equal about 120 calories. ( b ) Nutritive Enema (according to Ewald). — Two or three eggs are beaten smooth with one tablespoonful of cold water and a little salt — as much as can be held on the point of a knife. Wheaten starch, as much as can be held on the point of a knife, is boiled with y 2 of a cup (100 gm.) of a 20 per cent, solution of grape sugar and one wineglass (150 gm.) of red wine added. Then the solu- tion is cooled to 30° R., and the eggs are stirred in slowly. One can add also one teaspoonful of meat peptone, but this is not absolutely necessary. Nutritive clysters are to be injected while at blood heat and in quantities of 250 gm. at a time. Previously the rectum must have been cleansed by a purgative clyster. The addition of grape sugar had better be omitted, since through it decomposition and irritations of the intestines arise (Wegele). It contains about 400 calories.* *In calculating the value in calories of the nutritive clysters it is to be noted that the amount of resorption is difficult to determine, since it depends upon the state of the intestines, the skill of the patient in retaining the enema, etc. It is therefore well to assume only one-half as resorbed. MISCELLANEOUS PREPARATIONS. 281 ( c ) Nutritive Clyster (according to Boas). — Warm 250 gm. of milk, stir with two yolks of eggs, one teaspoonful of common salt, and one tablespoonful of wheaten starch, and afterward add one tablespoonful of red wine. If the mucous membrane of the rectum is easily irritated, one may add four to five drops of tincture of opium. Such clysters may be administered from one to four times in twenty-four hours (heated to blood heat), with a long, soft, rectal tube and a Heger’s funnel. Contains about four hundred calories. (d) Meat Bouillon-wine Clyster (according to Fleiner). — This consists of eighty gm. of beef-tea and forty gm. of mild white wine ; to be injected two or three times a day at body-heat. According to Fleiner, these clysters bring sleep to weakened patients. 7. Alcoholic Pancreas Extract ( according to Dr. Reichmart). — A fresh ox pancreas is freed from fat and skin immediately after kill- ing, chopped up, and y 2 of a liter of 12 to 15 per cent, alcohol is poured over. Let stand two to three days in a cool place, and filter. One wineglass for each meal. The following is a meat food recommended in the absence of secretion of hydrochloric acid : Meat Dumplings with Sardelle Dressing ( according to Mrs. J. C. Hemmeter). — Take ^ of a cup of finely scraped beef, ^ of a cup of lean pork ground through the meat-chopper. Add salt and a small amount of nutmeg; 2^3 ounces of butter creamed, yolks of two eggs creamed ; two ounces of stale bread soaked in cold water; after it is softened press it dry and add to the meat ; then add the beaten white of two eggs and mix all thoroughly. Turn into thirty dumplings and boil for five minutes. Dressing. — Take one cup of beef bouillon, add four sardelles scraped fine, the juice of ^ of a lemon and boil this for ten min- utes. Thereafter add y 2 of a glass of white wine, one teaspoonful of cornstarch, lastly the yolks of two eggs stirred in a little water ; then strain and pour over the dumplings. Serve only in a covered tureen. Gelatin Cream [according to Mrs. J. C. Hemmeter) for Anacidity Without Symptoms of Stagnation. — Juice of two oranges and one lemon (a little flavor of vanilla extract may be added if made for the healthy), y of a pound of sugar ; stir well and then add one pint of cream and beat until thick. Dissolve y 2 of a box of gelatin in y 2 of a pint of cold water; heat very gradually until all is thin 19 282 REST AND EXERCISE OF THE STOMACH. and dissolved. When cool add the cream, and beat until it is stiff. May be poured into a mold and given any shape.* THE USE AND ABUSE OF REST AND EXERCISE FOR THE DIGESTIVE ORGANS. In this connection we may consider rest and exercise before and after meals in reference to the entire body, and rest and exercise as applicable to the stomach and intestines only. Bodily exercise increases metabolism and therefore the appetite, and gives rise to a greater demand for food, but when it is carried too far, as in the overtrained athlete, fatigue may ensue and the appetite disappear entirely. Concerning the frequent question whether one should sleep after taking meals or not, or take exercise, much diversity of opinion exists. The edict of the Medical School of Salermo was : “ Post coenam stabis aut passus mille meabis,” which the Germans have translated as follows : “ Nach dem Essen sollst du stehn oder tausend Schritte gehn ” (“ After eating thou shalt stand or walk 1000 steps ”). This question is not easy to decide either way, for sleep reduces the peristaltic energy of the stomach, and thereby reduces the rate of digestion. A healthy person during sleep is robbed of the impetus which deep breathing imparts to the stomach by descent of the diaphragm. For most digestive sufferers, however, all bodily exercise, even moderate movements following immediately on large meals, con- stitutes more or less of a torment. In all conditions of gastric atony and myasthenia bodily rest is indispensable, because the stomach empties itself easier in the reclining position. Excepting in conditions of pronounced obesity and arteriosclerosis, I gener- ally permit an hour of sleep after the larger meals in all dyspeptic diseases. Blood pressure is increased during the digestive act, and for that reason sleep in a horizontal position is preferably avoided in the two conditions which I have excluded. Physical exertion, bathing, or training immediately after meals is not to be advised, because it may exert undue pressure upon the stomach, and divert the blood which this organ requires to the overactive muscles. Reading or writing after meals may be harmful for three reasons : * The author is greatly indebted to Mrs. J. C. Hemmeter for compiling and testing many of the most important recipes in the “ Dietetic Kitchen.” THERAPY OF REST AND EXERCISE. 283 1. Because it compels a wrong position of the body, inclining it too much forward. 2. Because of possible compression of the region of the stomach, due to cramped position or to pressing against the edge of the table. 3. Because of mental exertion. All psychic or emotional excitement immediately before, during, or after meals is harmful, and it is best not to eat at all, if the mind is occupied with some distressing thought. All gastric sufferers in whom neurasthenia is a factor should rest after meals, and those with pronounced neurasthenia should be permitted to sleep, for during sleep nervous energy accumulates and this may aid in restoring the lost digestive power. In all patients with motor insufficiency of the first degree I prefer to order sleep after meals. In the second and third degrees of this mechanical defect rest in bed becomes imperative. All anatomical diseases of the stomach require rest, and in ulcer, cancer, and acute gastritis rest is a “ sine qua non.” Mental Rest. — A large number of men of high intellectual ca- pacity are gastric sufferers. This comes from the universal abuse of the mental energies contemporaneous with overtaxing the di- gestive organ. The cerebral rest during and after meals is more imperative than muscular rest. Dyspeptics ought not to read their mail or papers before meals, lest some emotional news be imparted, reducing the appetite of these impressionable patients. Many gastric atonies are fundamentally caused by an overwrought ner- vous system. This one, almost universal, modern, bad habit of overtaxing the brain and nerves is a more dangerous and frequent cause, lying unknown and unrecognized at the foundation of many incipient gastric diseases, than all others put together. Dietetic Exercise. — Some forms of gastric disease do not re- quire any extraordinary amount of rest. It is not very easy to define, exactly, in just which cases exercise of the stomach is re- quired (as by administration of carefully adapted diet), and which cases require comparative rest. There is a form of chronic gastritis, of very slow progression, in which there is a slow atrophy of the oxyntic and ferment cells in the peptic ducts. I have watched cases of this type off and on for twelve years, and have learned by experience that a sparing diet and too much rest favors the progress of the atrophy, whereas a proportionate amount of food to keep up the caloric equilibrium will keep the peptic cells at 284 DIETETIC GYMNASTICS. work; for work in this case means growth and sustenance to the histological elements of the gastric mucosa. It is a mistake in those cases to level down the diet to the digestive capacity of the stomach. It should rather be leveled up, until the digestion can effectually deal with the amount of food required to maintain the nitrogen balance. It would be just as fatal a mistake to treat such a stomach by repose (few and small meals requiring little digestive work) as it would be to treat a mitral regurgitation with relaxed ventricular walls by absolute repose and exclusion of exercise. The modern conception of heart disease teaches that the stronger the ventricular wall can be developed, the sooner we can bring on a muscular hypertrophy, the more effectively will com- pensation be established and the patient have comparative free- dom from the consequences of his valvular insufficiency (Schott- Nauheim treatment for heart diseases). The forms of chronic gas- tritis that I refer to are always associated with a good motility, so that there is no stagnation or retention of food at any time. In purely nervous anorexia the appetite can be restored more effec- tively by feeding; in fact, if the disease is persistent and expresses itself by absolute refusal of food, it had best be treated by forced feeding. (See p. 190.) In hyperesthesia and achylia gastrica dietetic gymnastics, when scientifically employed in the manner described, are sometimes more beneficial than indiscriminate rest. In all cases where the tonicity of the gastric muscularis is re- duced, and in cases of gastroptosis and vertical position of the stomach the meals should be small in quantity and all bodily movements after the meals must be avoided. Kussmaul (S. Fleiner, “ Samml. klin. Vortr.,” Neue Folge, No. 103) has called attention to the fact that large meals and abundant ingestion of liquids, when such abnormalities of position and size of the stomach exist, may cause a transient mechanical obstruction of the duodenum. This occurs particularly if exercise is taken after the meals and the body kept in an erect position, which causes a stretching and dragging of the greater curvature. The heavily loaded pyloric portion of the stomach sinks and drags along the movable first portion of the duodenum, but at the place where the duodenum is rigidly fixed to the spinal column the bowel becomes kinked off. (See Anatomy of Duodenum, p. 39.) Therefore, in all forms of dilatation and abnormal positions of the stomach, physical rest of the body after meals, and as much AMERICANS EAT TOO MUCH. 285 physiological rest of the stomach as can be consistently given, is imperative.* The most explicit recent exposition of the physiological action of rest to the digestive organs and the prolonged substitution of exclusive rectal alimentation for gastric alimentation, is found in a book, by Dr. A. P. Gros (“ Traitement de Certaines Maladies de LEstomac par la Cure de Repos Absolu et Prolonge de L Estomac Avec Alimentation Rectale Exclusive ,” Paris, 1898). This valuable book contains a complete history of rectal feeding for the treat- ment of gastric diseases; the technics and the indications for such treatment and an exhaustive bibliography of the subject extending over nine pages. Dr. Gros has employed this rest treatment not only in ulcer of the stomach with and without hematemesis, but also in hypersecretion, in hyperacidity of long standing, in gastric catarrh with nervous anorexia, in the vomiting of pregnancy, and in the stenoses of pylorus of diverse origin. From a great many observations which I have made on persons living at hotels, etc., I have concluded, by approximate determina- tion of the amount of calories contained in their daily food, that the average American in the better classes of life eats entirely too much. Of course, it was possible to get at the caloric value of the food only approximately, but allowing the widest margin for possible sources of error, I found that the average number of calories rep- resented in the food taken was four thousand and forty per day for the average adult observed. This, of course, represents only the classes of individuals who can live at hotels of the better standard. As the amount of caloric energy required for a man of moderate muscular work is only thirty-five hundred, the excess of food taken is very evident. When sickness comes on, the common error is frequently made to introduce more food if possible than in health, on the supposition that the weakened body requires strengthening. This excess of good food and wine in our modern treatment of disease is as pernicious as the bleeding, vomiting, purging, and sweating of our medical ancestors. In an interesting little book, by Dr. Dewey, of Meadville, Pa., entitled “The True Science of Living” (Henry Bill Publishing * The value of rest to the stomach and rest to the body in diseases of the digestive organs is forcibly set forth in a contribution by Dr. C. D. Spivalc (“ Rest — A Neglected Factor in the Treatment of Gastro-intestinal Disorder,” “The Journal of the American Medical Association,” July 30, 1897). 286 TWO MEALS A DAY. Company, London, 1895), it is advised that temporary complete starvation until there is once more a healthy appetite is the best cure for a host of dyspepsias, debilities, bodily and mental depres- sions, headaches, etc., and that for similar less severe disturbances of nutrition the great remedy is to leave out the breakfast, so as to give the stomach a long rest of sixteen hours or more, with the object of allowing it to recuperate and accumulate secretory energy after the last meal of the previous day. One can not fail to be im- pressed with the force of Dr. Dewey’s logic and the correctness of his main contention. I have frequently put this matter to a test in private practice, but instead of omitting the breakfast I advise excluding the supper. The breakfast is taken at 8 a. m. and the dinner at 2 p. m. This was preferred because a large number of my patients were hard-worked business men and it was considered in- expedient to permit them to go the entire morning on an empty stomach. Six hours after the dinner, between 8 and 9 p. m., I order the stomach thoroughly washed out, and the patient retires on a perfectly empty clean stomach, and the organ is given twelve hours of absolute rest to store up its physiological energy. Curiously enough, the quantity of food taken, when only two meals a day are allowed in this manner, is often somewhat increased beyond the amount which was hitherto taken in three meals. Digestion is more perfect, the appetite is keener, nutrition is stimu- lated. On the recommendation of Alexander Haig (“ Uric Acid as a Causation of Disease, ” fourth edition, London, 1897, p. 628), who found this plan a most powerful stimulant to digestion and nutrition, I made a thorough trial of Dr. Dewey’s suggestion on my own person, with the result that at present I still carry out the two-meal-per-day plan. Resting the stomach will enable it to do much better work and leads to a keen hunger otherwise unknown. Haig concludes that if anything will demonstrate the insane folly of stuffing a dyspep- tic stomach with fresh food every three or four hours, an experi- ence of this kind ought to do it, and I can confirm his suggestion that almost the only danger attendant on taking two meals a day, in place of three or four, is that of overeating. The two-meal-a- day plan is one of the most effective means of combatting intes- tinal flatus which arises from undigested residues. It is quite possible for a man to be better nourished on a little food eaten slowly and well mixed with saliva than on a great deal of food eaten very quickly. I have seen a number of cases where persons DIETETICS OF ALCOHOL. 287 seemed undernourished on three to four meals a day who gained weight and showed a better appetite, and no undigestible residues in the stools when but two meals a day were allowed. It is quite conceivable that persons may be in a state of starvation, not from any want of food, but from the fact that the digestive capacity is constantly overpowered by excess of food. The so-called uric-acid- free diet, which Haig urgently recommends in form of a diet con- sisting almost exclusively from substances derived from the vege- table kingdom, is, in my experience, not universally applicable to digestive diseases. It should, however, be more employed than it has been hitherto, particularly in those stomach affections asso- ciated with hyperacidity. In the beginning no surprising bene- ficial results may be evident, but the success of the treatment depends on the persistency with which it is carried out. Haig permits the use of milk, butter, and cheese, but forbids meats of any kind. CHAPTER III. THE DIETETICS OF ALCOHOL AND ALCOHOLIC BEVERAGES. The literature on the subject of the physiological action and the metabolic and dietetic influences of alcohol is very extensive. Its abnormal growth appears to those who make an effort to keep abreast of the progress and advancement of experimental thera- peutics, out of all proportion to any real increase in our knowledge of the subject. We are directly concerned only with the (1) value (if any) of alcohol as a food; (2) as a tonic and stimulant; (3) its effects upon the digestive functions. The use of alcohol in any shape is wholly unnecessary for the use of the human organism in health. A large number of persons prolong their lives by total abstinence. This should be so stated with emphasis, since there are so many who imagine it is indispensable, when in reality they are injured by it. The effects of alcohol on other organs than the stomach are very important ; but we must refer to the literature on the special experiments : For the influence 288 DIETETICS OF ALCOHOLIC BEVERAGES. of C 2 H 6 0 on the heart, see J. C. Hemmeter, “ The Comparative Physiological Effects of the Ethylic Alcohol Series on the Isolated Mammalian Heart” (in “Studies from the Biological Laboratory of the Johns Hopkins University,” vol. iv, No. 5). On the value of alcohol on various body functions,, see Gilman Thompson, “ Dietetics,” pages 205 to 232 ; Binz, “ Pharma- kologie”; Schmiedeberg, “ Arzneimittellehre.” The literature on the effect of alcohol on the functions of the stomach can be found in the text-books of Riegel, Boas, Ewald, Wegele, Pen- zoldt (vol. iv of “ Handbuch d. Therapie ”), Munk,and Uffelmann. The literature is too great and the results are too uncertain to permit of any resume to be given here. The question arises, “ Why do we give alcohol in gastric therapeutics ? Is it a food or merely a stimulant ? In doses taken ordinarily with the more common beverages does it facilitate or retard digestion ? ” Most of the text-books mentioned take the stand that as alcohol is oxidized in the body it furnishes a considerable amount of energy. The question whether alcohol is a true food-stuff, capable of serving as a direct source of energy and of replacing a correspond- ing amount of fats or of carbohydrates in the daily diet, is a matter of controversy. Reichert (“Therapeutic Gazette,” Feb. 15, 1890) concludes that moderate doses of alcohol do not affect the total amount of heat produced in the body of a dog. As it is nearly completely oxidized in the body, and gives off considerable heat in the process, the fact that the total heat production remains unaltered indicates that the oxidation of alcohol protects an isody- namic amount of food-materials in the body from consumption, thus acting as a food-stuff capable of replacing other elements of the food. Opposed diametrically to these results are those of Miura (“ Zeitschr. f. klin. Medicin,” 1892, vol. xx, p. 137), whose obser- vations were made on his own metabolism, after he had brought himself into a condition of nitrogen equilibrium upon a mixed diet. Then for a time a portion of the carbohydrates was omitted, and its place substituted by an isodynamic amount of alcohol. The result was a loss of proteid from the body, proving that the alcohol had not protected the proteid tissue as it should have done if it acts as a food. In a third period the old diet was resumed, and after nitrogen equilibrium had again been established, the same proportion of carbohydrates was omitted from the diet, but alco- hol was not substituted. When the diet was poor in proteid, it was found that less proteid EFFECT OF ALCOHOL ON METABOLISM. 289 was lost from the body when alcohol was omitted than when it was used, indicating that so far from protecting the tissues of the body by its oxidation, the alcohol exercised a directly injurious effect upon proteid consumption. Recent experimental investiga- tions (Rosemann, “ Ueber d. Einfluss des Alkohols auf den mensch- lichen Stoffwechsel,” “ Zeitschr. f. Diatet. u. physikal. Therapie,” von Leyden u. Goldscheider, Bd. 1, p. 138) confirm Miura’s results, namely, that alcohol is no proteid saver, but protects the fats from consumption. Further researches will have to show whether and how it protects the oxidization of non-nitrogenous constituents of the body — the fats. Professor W. O. Atwater, from experiments on the effect of alco- hol on metabolism, conducted in a thoroughly scientific and sys- tematic manner at the Wesleyan University, concludes : 1. The alcohol is oxidized — that is, burned — as completely as bread, meat, or any other food. 2. In the oxidation all the potential energy of the alcohol was transformed into heat and muscular power. In other words, the body made the same use of the energy of the alcohol as of that of sugar, starch, and other ordinary food materials. 3. The alcohol protected the material of the body from consump- tion just as effectively as the corresponding amounts of sugar and starch — that is to say, whether the body was at rest or at work, it held its own just as well with the one as with the other. According to Atwater, alcohol is not a tissue builder, but it can and does serve as fuel. The amount used in his experiments per day was equal to about 2 y 2 ounces of absolute alcohol — about as much as would be contained in five or six ounces of whisky or in a quart of claret or Rhine wine. (Extract from “ Report to Mid- dletown (Conn.) Scientific Assoc.”; the experiments have not yet been published.) It is emphasized that alcohol is not a desirable food for common use ; for in saving the non-nitrogenous bodies (the fats) from con- sumption — an observation which agrees well with the practical experiences concerning the habitual use of alcohol — it is very probable that alcohol acts as a weak protoplasmic- poison. Miura ( loc . cit.) has already suggested such an influence; also Romeyn (see Maly’s “ Yahresbericht d. Thierchemie,” 1887, p. 400), Stammreich (“ Inaug. Dissert.,” Berlin, 91), and A. Schmidt (“ Centralbl. f. d. Med. Wiss.,” 1875, No. 23). The work of these four experimenters showed an increased albumin breakdown, which in Miura and 290 DIETETICS OF ALCOHOLIC BEVERAGES. Stammreich’s observations continued for two days after the use of alcohol had been stopped. The results of Atwater do not support the assumption that alcohol may be used as a food ; they indicate that it protects the oxidation of the fats. Saving the fats from consumption, even if it could be accomplished without injurious collateral effects, is, from a therapeutic standpoint, only very rarely desirable (emaciation, tuberculosis). But if it is accompanied by increased destruction of the proteids of the body, then alcohol is not a dietetic aid for the advancement of nutrition. Therapeutically, there is still conceded to alcohol a stimulating and an antipyretic influence. Concerning the effects of moderate amounts of alcohol on diges- tion by pepsin-hydrochloric acid, and on salivary and pancreatic digestion, we believe the following abstract of Chittenden and Mendel’s experiments (“ American Journal of Medical Sciences,” January to April, 1896) to be a clear representation of this matter: One can not define with mathematical exactness the action of a given percentage of absolute alcohol on pepsin proteolysis, since variation in the attendant conditions, i. e., the relative amounts of pepsin, acid, and proteid, together with the period of digestion, the digestibility of the particular proteid, etc., are prone to modify the final result. Thus, with a weak gastric juice, where the amount of ferment present is small, and digestive action consequently slow, or where the proteid material used is difficult of digestion, the re- tarding effect of a given percentage of alcohol is far greater than when the digestive fluid is more active ; that is, when it contains more pepsin. Further, this difference of action is more pronounced the larger the percentage of alcohol present. The following gen- eral conclusions were drawn from artificial digestive mixtures. First. It is plainly manifest that in the presence of small amounts of alcohol (one to two per cent, of absolute alcohol) gastric diges- tion may proceed as well or even better than under normal circum- stances. In fact, many of their experiments show a slight increase in digestive power when the mixture contained one or two per cent, of absolute alcohol. This increased digestive action, though slight, occurred too frequently to be the result of mere accident, and apparently indicates a tendency for alcohol, when present in small quantity, to slightly increase the digestive action of pepsin-hydrochloric acid; or, in other words, to stimulate the ferment so that it can accomplish somewhat more than it other- wise could do. As the percentage of alcohol is raised, retardation ACTION OF ALCOHOL ON PANCREATIC DIGESTION. 29 1 or inhibition becomes more noticeable, although ordinarily it is not very pronounced until the digestive mixture contains five to ten per cent, of absolute alcohol. With 15 to 18 per cent, of absolute alcohol digestive action may be reduced one-quarter, or even one- third ; the exact amount of retardation, however, being especially dependent upon the activity of the gastric juice and upon the natural digestibility of the proteid material. It is to be remem- bered, however, that 18 per cent, of absolute alcohol would be equivalent to 36 per cent, of proof-spirit; so that, if we could assume the contents of the human stomach at a given period to contain one-third proof-spirit, it might perhaps be considered that digestive action would be retarded to the extent of 25 to 35 per cent., provided the gastric juice present in the stomach was of fair strength and the proteid matter of ordinary digestibility. Such percentages of proof-spirit, however, are not likely to be long present in the stomach, and it is perhaps idle to speculate on such hypothetical cases. We may in this connection, however, again emphasize the fact that the stronger the gastric juice and the more digestible the proteid food undergoing digestion, the less re- tardation will a given percentage of alcohol produce ; while, on the other hand, the weaker the gastric juice and the more indi- gestible the proteid, the greater will be the inhibition caused by a given percentage of alcohol. In other words, those variations which must naturally exist in the stomach contents of different in- dividuals, both in health and disease, will lead to different degrees of retardation in the presence of given percentages of absolute alcohol. It would, therefore, be unwise to make a general specific statement regarding the action of a given percentage of alcohol. Under definite conditions, however, as Chittenden’s experiments plainly show, the presence of a definite amount of alcohol always leads to essentially the same results. In order to prevent any misinterpretation of these results, we would again call attention to the fact that we are dealing here with only one of the four questions that need to be answered before we can hope to fully understand the influence of alcohol on gastric digestion as a whole. Thus, the results afford plain evidence of the influence of alcohol on the digestive or solvent power of the gastric juice ; but we should not be justified in arguing that exactly the same results would follow from the introduction of alcohol into the living stomach. The action of a given percentage of alcohol on proteolysis alone would be essentially the same in the stomach 292 DIETETICS OF ALCOHOLIC BEVERAGES. as in a beaker, provided the alcohol was not absorbed into the blood and thus removed from contact with the digestive mixture, and provided it did not exert any influence on the character of the gastric juice secreted. But it is easily conceivable that a percent- age of alcohol which does not interfere with solution of the proteid food-stuffs may so modify the amount or character of the secretion that digestion might be greatly stimulated or greatly retarded. Further, as already stated, the presence of alcohol in the stomach may so affect absorption and peristalsis that the rate of digestion may be modified from this cause ; hence the results above recorded are to be used only in drawing conclusions as to the effect of vari- ous percentages of alcohol on the purely chemical process of gastric digestion, i. e ., on pepsin-proteolysis. In conclusion, it is to be noted that Chittenden’s results are more or less in accord with what has been previously published concerning the action of alcohol on gastric digestion. Thus, Bikfalvi found, in artificial digestive experiments, that alcohol, even in small quantities, retards normal gastric digestion. Klikowicz found that the presence of five per cent, of alcohol in the digestion of egg- and serum-albumin led to somewhat variable results, although, as a rule, there was an indication of a slight stimulation of proteolytic action. In the presence of ten per cent, of alcohol there was always marked retardation, while fifteen, twenty, and thirty per cent, of alcohol checked digestion to a marked degree. Roberts found, by artificial-digestion experiments, that in the presence of less than ten per cent, of proof-spirit there was no appreciable retardation. With ten per cent., retardation was only barely detectable. With twenty per cent, there was quite distinct but still only a slight retardation. Above this point, however, the inhibitory effect of alcohol increased rapidly. (Refer to the tables of Roberts at the end of this chapter.) That the action of a digestive ferment may be both stimulated and retarded by the same sub- stance, according to the quantity present, has been already demon- strated ; hence there is no inconsistency in the above results with alcohol. The same action has likewise been observed with yeast- cells. Action of Alcohol on Pancreatic Digestion. — In view of the position which pancreatic digestion occupies in the digestive proc- ess, it is readily seen that it is more desirable to ascertain the influence of small quantities of alcoholic liquors than large amounts, since absorption must naturally lead to a decided dimi- EFFECT OF ALCOHOL ON ABSORPTION. 293 nution of alcohol before it can normally become mixed with the pancreatic juice and partially digested food-material in the small intestine. Hence, more stress was, as a rule, laid upon the influence of small percentages of the various fluids experimented with, and only occasionally the action of large quantities was tried. The results with absolute alcohol indicate that the proteolytic ferment of the pancreatic juice is more sensitive to absolute alcohol than the ferment of the gastric juice. Retardation of digestive action is more pronounced, even with small amounts of alcohol. Further, as in the case with pepsin, the weaker the digestive powers of the pancreatic juice, the greater the retarding action of absolute alcohol. When the amount of alcohol present in the digesting mixture is less than one per cent, the retardation of the digestive action is very slight, provided the ferment is fairly vigorous in its action. Action of Alcohol on Salivary Digestion. — In the first set of experiments on salivary digestion Chittenden determined the time it took to reach the achromic point. By this method he found that absolute alcohol has very little influence upon the amylolytic or starch-digesting power of neutral saliva. Only when the saliva, added to the digestive mixture, is diluted in the proportion of 1 : 30, does the presence of even ten per cent, of alcohol have any measurable influence, and then only to retard the appearance of the achromic point two minutes. As this percentage of absolute alcohol is equal to at least twenty per cent, of proof-spirit, it fol- lows that pure alcohol free from admixture is practically without influence upon the digestion of farinaceous food by the saliva. By the second method, which was to determine the amount of maltose formed, he found that small amounts of absolute alcohol may actually cause an increased formation of maltose. On the other hand, the presence of ten or fifteen per cent, of absolute alcohol leads to a distinct retardation in the formation of sugar, although the inhibition is not very great considering the amount of alcohol present. This retardation of the secondary action of the ferment is perhaps suggested by the slight delay in the appearance of the achromic point in the presence of ten per cent, of absolute alcohol. Effect of Alcohol on Gastric Peristalsis. — We have personally made a number of observations concerning this special point on three healthy students with normal stomachs by means of our method of graphically registering the gastric peristalsis on the 294 DIETETICS OF ALCOHOLIC BEVERAGES. kymographion (“ New York Med. Journal,” June 22, 1895). These students were teetotalers, and to exclude the influence of suggestion the alcohol was poured into the stomach, diluted, through a tube, and sometimes water was used in place of alcohol. The subject was at no time aware of what was being used. It was found that alcohol, when contained in gastric contents up to six per cent., exerts no appreciable effect on the motility one way or the other ; but beyond this the peristalsis begins to show evidence of im- pairment. The presence of twenty to twenty-five per cent, of alcohol leads to a very distinct retardation and reduction of the tonicity in the gastric movements, which seems to last in its effects from two to three hours. Even after the alcohol is thoroughly washed out of the stomach the peristalsis continues to be retarded. In dogs the identical results were obtained, except that at five to six percent, a short period of peristaltic unrest was observed before the marked inhibition developed. The inhibition of the peristalsis when the gastric contents contain twenty to twenty-five per cent, of alcohol occurs quite regularly, and is not the result of mere accident. It is probably due to a direct poisoning effect on the muscularis, similar to the poisoning effect on the heart-muscle observed by us (Hemmeter, “ Studies from the Biological Labora- tory,” loc. cit .). This amount of alcohol must be in the organ at least ten minutes before the peristaltic inhibition sets in. Effect on Absorption. — The effect of alcohol on the rate of absorption from the stomach is a different question from the absorbability of the substance itself. There is a general unanimity that, owing to its rapid diffusibility, alcohol is promptly absorbed from mucous surfaces. At the same time the experiments of von Mehring suggest that the absorption of substances soluble in alcohol may be facilitated by the latter; for example, that peptone or maltose taken in alcohol may be absorbed more rapidly than when taken in water. Exact experimental facts concerning this matter are wanting. In large doses alcohol hinders absorption by the direct damage it does to the cylindrical surface epithelium. Among gastro-enterologists the impression prevails that alcohol and alcoholic beverages are capable of promoting the appetite; and probably for this purpose and for its stimulating effect we are justi- fied in giving it. Summing up the physiological action, so far as we are concerned, it may be said : (1) The effect of moderate doses EFFECT OF MALT LIQUORS ON GASTRIC DIGESTION. 2Q5 of alcohol on metabolism is that it not only fails to protect proteid oxidation, but actually increases it. Oxidation of fat is probably inhibited. (2) That on pepsin hydrochloric acid it acts favorably in quantities equal to one to two per cent, of absolute C 2 H 0 O, but beyond that it gradually inhibits this action. (3) On pan- creatic digestion it acts unfavorably. (4) On salivary digestion it acts favorably, increasing the formation of maltose when present in amounts not exceeding five per cent. (5) On the peristalsis it has no influence until the amount exceeds six per cent., when it begins to inhibit the motility. (6) Its effect on the rate of absorp- tion is unknown. In pathological conditions the effects of alcohol are undeniably different, its stimulating and temperature-depressing influence mak- ing it of value in continued fevers. In pathological cases, wher- ever the amount of free HC 1 is altered, either in hyperchylia or achylia gastrica, Chittenden’s deductions do not hold good. In hypochylia, or subacidity, alcohol may be of some service in stimu- lating the mucosa to more prolific secretion, but in hyperchylia it irritates the already very much excited gland-cells still further. In achylia with entire absence of secretion, digestion is considerably reduced by alcohol. Speaking generally, alcohol might be dis- pensed with as a therapeutic and dietetic agent if it were not for its appetizing, stimulating, and antipyretic qualities. In hyper- acidity and hypersecretion, in ulcer and all chronic affections with augmented secretion, alcohol is contraindicated. In atonic stom- achs with retention and stagnation of contents and pronounced impairment of motility alcohol, in our experience, acts as a poison. Symptoms of vertigo, nausea, and even tetany are directly trace- able to the introduction of whisky or wine under such conditions. In our opinion these results are brought about by substances already existing in these types of stomach diseases, which are prevented from entering the circulation by a protective action of the gastric mucosa, which does not absorb them. The addition of alcohol renders these toxins absorbable. Healthy stomachs not rarely exhibit a certain adaptation to alcohol, and, naturally, upon such organs the agent has a different effect than upon the stomach of a teetotaler. Beer has a very little therapeutic utility ; by reason of its weight it is contraindicated in all conditions weakening the gastric wall. Riegel holds that it is well to permit its use in simple hyperacidity. It contains a certain amount of nutritious matter, and should, 296 DIETETICS OF ALCOHOLIC BEVERAGES.* therefore, not be forbidden if the patient craves it, provided the motor power is good. Even the absorption of less bulky wines is attended by an excretion of water into the stomach (von Mehring, loc. cit.), which may favor stasis of liquids and furtherance of existing dilatation. The following is a table by Roberts (“ Lectures on Dietetics and Dyspepsia ”), showing the effects of various percentages of malt liquors on gastric digestion : Proportion of Malt Liquors in the Digesting Mixture. Time in which Digestion was Completed (Normal, One Hundred Minutes). Ale, Burton. Light English Table Beer. , Lager Beer. Ten percent., 1 15 minutes, . . 100 minutes, . . 100 minutes. Twenty per cent., 140 “ 115 “ • • 115 “ Forty per cent. 200 “ . . 140 “ 140 “ Sixty per cent , Embarrassed, . 180 “ 180 “ The digesting mixture contained two gm. of dried-beef fiber, 0.15 percent, of hydrochloric acid (HC 1 ), and one c.c. of glycerin, extract of pepsin, and varying quantities either of wines or malt liquors, and filling up to 100 c.c. with water. The following table gives the effects of various percentages of hock, claret, and champagne upon peptic digestion (Roberts) : Proportion of Hock, Claret, or Champagne in the Digesting Mixture. Time in which Digestion w t as Completed (Normal, One Hundred Minutes). Hock. Claret. Champagne. Ten percent., 100 minutes, . . . 100 minutes, . . 90 minutes. Twenty per cent., 115 , . | 140 “ 100 “ Forty per cent., 150 “ . . 180 “ . . 130 Sixty per cent. Embarrassed, . Embarrassed, . 180 “ In cases of gastric disease where great general debility commands liberal alcoholic stimulation, particularly if the gastric motor func- tion be impaired, it is best to administer the stimulant by rectal enema. It may have been observed that most of the enemata have provided for this emergency, and contain more or less wine. Sir Wm. Roberts points out that in the plan of the dietary of the civilized races, arrived at slowly, as the result of an immense experience, we seem to detect two apparently contradictory aims — LAVAGE AND THE GASTRIC DOUCHE. 297 namely, on the one hand, to render food, by preparation and cooking, as digestible as possible; and, on the other hand, to control the rate of digestion by the use of certain accessory articles with food, such as alcoholic beverages. In reality these objects are not contradictory, but cooperative to a beneficial end. For, to express the problem in another way, it may be said that we render food, by preparation, as capable as possible of being completely exhausted of its nutrient properties ; and, on the other hand, to prevent this nutrient matter from being wastefully hurried through the body we make use of agents which abate the speed of diges- tion. This combination of appliances renders our plan of feeding more elastic, more adaptable to variety of individual health and constitution, and to variety of external conditions. If this view of digestive retardation in the stomach be well founded, the stomach becomes in some degree a storage organ for food — like the crop of birds, the paunch of ruminants, the dilata- ble cheeks of monkeys, and the pouch of the pelican. This classical writer on dietetics expresses himself similarly on the importance of preparing the food in such a way that it tastes good (Sir William Roberts, loc. cit ., “ The Eulogium of the Pal- ate ”). Even Bunge, the well-known physiologist, who is a pro- nounced teetotaler, declares that we are justified in the use of any food or drink if for no other reason but that it gratifies the palate, provided it does no harm ; but the substitution of harmless food and drink for alcohol is strongly urged. CHAPTER IV. LAVAGE AND THE GASTRIC DOUCHE. The technics of lavage — the indications for and against it — have been treated in the section on the Stomach-tube. In brief, lavage is indicated (a) where the exit of the chyme from the stomach is hindered by a mechanical obstruction, giving rise to decomposi- tions. To this class belong all forms of dilatation except those depending on simple atony, for here we are not dealing with any obstruction to the outflow, but with a lowering of the peristalsis, which is not markedly benefited by lavage. Dilatations that indi- 20 298 LAVAGE AND THE GASTRIC DOUCHE. cate lavage are those due to cicatricial stenosis, or neoplasm of the pylorus and duodenum, and impairment of motor function in consequence of carcinoma, sarcoma, syphilitic and tuberculous gastritis, simple atrophic gastritis, myasthenia, contractions caused by acids, alkalies, or other chemicals. The benefit derived from lavage must vary with the stage at which the treatment is undertaken. In cases of cicatricial stenosis of mild and incipient character the dilatations have been cured by lavage, probably because a compensatory hypertrophy of the musculature, develop- ing gradually, enabled the organ to expel the chyme. In these gastrectasias the stomach, after the systematic lavage treatment, no longer contained food and HC1 in large quantities in the morning. The stools and the quantity of the urine became normal, and the patients could tolerate an ordinary diet. But such cases must, even after recovery, avoid overloading the stomach, as this has been known to bring about relapse. The compensatory hyper- trophy of the musculature, although it may last for years, in these cases is not a permanent condition, and in our experience often gives way to a subsequent atrophy and return of all the symptoms of stagnation. ( b ) The second main indication is where foreign or irritating collections are mixed with the gastric contents, which sooner or later interfere with digestion. These collections may consist of abnormally augmented gastric juice, of gastric, pharyngeal, and esophageal mucus, and of bile. In hypersecretion lavage is best carried out with sodium bicarbonate, and thereafter with argentic nitrate or bismuth subnitrate. The pyrosis, distention, and consti- pation are much relieved thereby. In cases of much accumulation of mucus, warm alkaline and saline solutions are preferable ; for in the gastritis mucosa the HC1 secretion is lost, and common salt is a stimulant to that secretion — if there be any secreting glandular cells left. I have found that sulphocarbolate of zinc, in the strength of one grain to one ounce of water, will check excessive secretion of mucus in chronic gastritis. It is used in the intragastric spray after previous lavage. Toxic products of complex nature may accumulate in the organ, in consequence of carcinoma, uremia, and diabetes mel- litus; here lavage is also indicated. During the lavage one should always have a second glass vessel, holding one liter, into which the outflow discharges, so that it may be ascertained each time how much is regained. It is very dangerous to wash out the stomach with medicated and antiseptic solutions without ascertaining THE GASTRIC DOUCHE. 299 whether all the solution flows out again. Even with simple water, overloading of the stomach can not be avoided except by measur- ing the outflow. In a paper published in the “ Practitioner” (1892, No. 4) W. Soltau Fenwick reports three cases of poisoning from leaving antiseptic solutions in the stomach. In one case (“ Schmidt’s Jahrbucher,” 1883, Bd. cxcvm, p. 28) death was caused in six days by leaving a two to three per cent, solution of boric acid in the stomach. Fenwick also makes a strong plea against the indiscrim- inate use of antiseptics within the stomach, for the alimentary canal is endowed with the power of absorbing not only the poisonous products of the bacteria, but also most of the substances which are introduced to destroy them (W. S. Fenwick, “ Disorders of Diges- tion in Infancy,” etc., p. 141). Tetany has been observed after lavage by Bouveret and Devic, who collected twenty-one cases (“ Revue de Med.,” February, 1892). In all, thirty-four such cases of tetany of gastric origin have been re- ported, though not all due to lavage. Ewald reported two cases that are of interest — one a male, aged forty-five, who died from a sud- den, copious, esophageal hemorrhage two days after he had sought relief by introduction of the esophageal sound. There were symp- toms of mediastinal tumor or aneurysm. The second patient died suddenly while he was intro- ducing the tube himself ; the autopsy showed a dissecting aneurysm at the beginning of the ascending aorta, still within the pericardium. Frerichs and Penzoldt have reported similar cases. Every new patient should, therefore, be examined for abnormal conditions within the thorax before lavage. The Gastric Douche. — By douching the stom- ach, is meant an internal irrigation with water .... T . Fig. 26.— Recurrent under high pressure. It was first practised at gastric needle ., ... . , . Spray or Douche. Kussmaul s clinic, and described later by Mal- branc (“ On the Treatment of Gastralgias by the Internal Gastric Douche,” etc., “ Berlin, klin. Wochenschr.,” 1878, No. 4). It does not differ essentially from ordinary lavage except in the fact that the funnel or vessel into which the water is poured is held at least one meter above the cardia. Rosenheim improved and revived 300 LAVAGE AND THE GASTRIC DOUCHE. the method, after it had been disregarded for twelve years, by de- vising a special douching tube with numerous very small, lower openings instead of one or two large ones. Water that is allowed to run into the stomach through such a tube under high pressure strikes the walls with many currents of considerable impetus. The central or terminal opening in Rosenheim’s douche tube is larger than the lateral ones, and permits of an easy outflow. Dr. F. B. Turck, of Chicago, has devised a stomach needle douche with a separate outflow tube ; it also produces an intragastric shower (Fig. 26), and is a useful instrument. Rosenheim recommends the douche for nervous dyspepsia and chronic gastritis, with or without impaired motility. If the douch- ing was done with solution of sodium chlorid an increase in the HC 1 production could be ascertained; whereas nitrate of silver caused a reduction of the secretion (“ Berlin. Klinik,” 1894, Heft 71). Riegel speaks well of argentic nitrate applied in this manner for all irritative states of secretion ( loc . cit., p. 300). Fleiner has called attention to the fact that he and Kussmaul could incite a feeling of hunger by douches. These clinicians increased the effect by irrigating the gastric mucosa with solutions of bitter tonics : hops and quassia were experimented with. In severe cases of anorexia we have tried this method with infu- sions of gentian and cinchona, and were pleased with the effects. Einhorn has invented an intragastric spray (Fig. 27), which is rec- ommended for disinfection of the mucosa, to produce an astringent or an anesthetic effect. It is surprising what a trifling amount of cocain is necessary to relieve a gastralgia when used in this manner. For gastric erosions the nitrate of silver spray (1 : 1000) is frequently curative. For excessive secretion of mucus zinc sulphocarbolate, one grain to one ounce of water, can be recom- ELECTRICITY IN THE TREATMENT OF GASTRIC DISEASES. 30 1 mended. The gastric douche and spray should be applied only in an empty stomach. Motor impairment of nervous origin is occasionally much improved by alternately douching with warm (ioo° C.) and cold water. Electricity in the Treatment of Gastric Diseases. — The effect of electricity on the various functions of the stomach has been already referred to under the consideration of the motor function and will be further described under the various diseases in which it is recommended. The results of physiological experiment and of clinical experience are largely contradictory. Physiological experiments, when conducted by medical men, are frequently inexact and misleading. It requires special physiological labora- tory training of years to control the technics of vivisection and general experimentation. In the experiments of medical men on the physiological effects of electricity it is not difficult to find numerous defects in the physics and physiology of the methods used, the conduct and the execution of the experiment, etc., which render their results invalid from the outset; so that it is useless to go into the literature of the history of gastric electrotherapy exhaustively. Many experimenters fail to give the details and conditions, the kind of cell used, the number of milliamperes, the number of faradic stimulations to the minute, the kind of electrode, the distance of primary from secondary coil. Control experiments are wanting to ascertain whether, in the same animal, peristalsis could not be observed per se without stimulation by electricity, or whether the stimulation may not have been purely mechanical, not electrical. From a clinical standpoint it is not necessary to demonstrate that electricity can produce changes in the chemistry, resorption, and motility of the stomach in order to justify its employment; for there may be, and probably are, influences exerted by elec- tricity upon the nutrition of living cells which as yet escape our methods of analysis. The effect of electrical stimulation of the cells of spinal ganglia, as seen and determined by micrometric measurement, and consisting in a loss of bulk mainly in the nuclei, was first described by C. F. Hodge, in the “ American Jour, of Psychology ” for May, 1888, and May, 1889. Judging from these experiments, which were conducted with exemplary accuracy and regard for physiological detail, it is reasonable to presume that, in some way or other, the metabolism of muscle-, gland-, and nerve- cells of the stomach may be influenced by electricity. The 302 LAVAGE AND THE GASTRIC DOUCHE. demonstration of this is a future prospect ; at present the main reason why we employ this agent is simply because we know that in certain diseases it is of much benefit. Physiology may come to our aid later on, and tell us why it is that these results are pro- duced. From the work done by medical physiologists so far, no clear deductions are possible. The electrical stimulation of the vagus in a subject, forty-five minutes after execution, which was carried out by Beynard and Loye (“ Progres Medicale,” 1885. No. 29), and produced a secre- tion of gastric juice, has strengthened the belief that the vagus contains gastric secretory fibers. Ziemssen (“ Klinische Vortrage,” No. 12, 1887), Rossi (“ Lo Sperim.,” 1881), and Hoffmann, who experimented at Riegel’s clinic (“ Berlin, klin. Wochenschr.,” 1889, No. 12), all arrived at the conclusion that electricity promoted the secretion of gastric juice. The results of investigations concerning the influence of the two kinds of currents — the constant and the interrupted — differ widely. Einhorn was of the opinion that the faradic current pro- moted secretion and the galvanic impeded it (“ Deutsche med. Wochenschr.,” 1893; also “ Zeitschr. f. klin. Med.,” Bd. xxiii). The experiments of Hoffmann ( loc . cit.) suggested that the galvanic current favored an increased secretion, while Bocci’s results with intragastric faradization would have us believe that in animals the interrupted current can augment both peristalsis and secretion (“ Lo Sperimentale,” Giugno, 1881). Concerning the effect of electricity on the motor function we might quote a few experimenters. Schillbach (“ Virchow’s Arch.,” Bd. cix, p. 284) produced strong contractions at the site of the anode by applying the galvanic current to the intestines of a rabbit. Von Ziemssen (loc. cit .), Bocci (loc. cit.) y Ludwig, and Weber have stated that the faradic as well as the galvanic current applied directly to the stomach cause contraction of the same in animals. Fubini (“ Centralbl. f. med. Wiss.,” 1882, No. 33) concluded that electricity accelerates intestinal peristalsis ; he experimented on Vella’s double intestinal fistula. Two Americans, Rockwell and Beard (“ Phila. Medical and Surgical Reporter,” 1868, No. 20), were among the first to employ electricity in the treatment of nervous dyspepsia. In Pepper’s case of spontaneous, visible, gastric peristalsis (‘‘Phila. Med. Times,” 1871, p. 274) no peristaltic movements could be produced by applying electricity percutaneously. Kuss- EFFECT OF ELECTRICITY ON GASTRIC PERISTALSIS. 303 maul, in 1877, stated that “ the therapeutic results obtained by Fiirstner in gastrectasias did not prove that an actual peristalsis was produced by the current, but they were probably due to con- traction of the abdominal muscles” (“ Archiv f. Psychiatrie u. Ner- venkrankh.,” 1878, p. 205). Canstatt first suggested treating dila- tations by placing one electrode in the esophagus, the other on the stomach ; and Duchenne first actually applied this method (both the latter quoted from Kussmaul, loc.cit .). In 1877 Kussmaul {Joe. cit.) began introducing intragastric electrodes, made by inserting a copper wire in a stomach-tube, the wire terminating in a little ex- posed knob which came in direct contact with the inner gastric surface. Fig. 28. — Rectal Electrode. Bardet improved this method by a similar electrode, which, how- ever, did not come in contact with the mucosa in one spot only, but by a quantity of water previously taken it was distributed over the entire surface (Bardet, “ Bull. Gen. de Therap.,” 1884). Ziemssen then employed a similar, device, but Einhorn completed the evolution of the intragastric electrode by originating a soft, very plastic, deglutable instrument, the end of which is inclosed in an ovoid, perforated, hard-rubber cap. Ewald prefers Einhorn’s elec- trode a little more rigid, so that it can be pushed into the stomach and need not necessarily be swallowed. The thickness of the rub- ber tube in Ewald’s modification is 1^ mm. Rosenheim (loc. cit.), Wegele (“ Therap. Monatshefte,” April, 1895), Charles G. Stockton 304 LAVAGE AND THE GASTRIC DOUCHE. (“ A New Gastric Electrode,” “ Medical Record,” Nov. 9, 1889), and F. B. Turck have later devised electrodes for this purpose which represent no advance over those mentioned. The thin-wired elec- trode of Einhorn (Fig. 29) possesses the advantage that it can be swallowed by those not used to the stomach-tube, to which they must become accustomed in case Wegele’s, Stockton’s, or Rosen- heim’s electrode is employed. The inclosing tube of Einhorn’s instrument is really too thin, however, for in our experience it rap- idly wears through near the connection with the hard-rubber end- cap, and we consider Ewald’s modification safer, more durable, and of easier introduction. These results correspond in the main with those previously pub- lished by Meltzer (“ New York Med. Jour.,” June 15, 1895), whose experiments were conducted with great care, and from a physio- logical aspect are beyond reproach. We should have preferred knowing how many vibrations to the second Meltzer used, since we have assured ourselves that when too many stimulations to the second are thrown into a muscle, particularly an involuntary mus- cle, it will not contract at all ; whereas the same muscle will con- tract if a smaller number of stimulations be used (judged by the Kronecker interrupter and a Jacquet chronograph). These facts were first stated in an article in the “ New York Med. Jour.” (Hem- meter, “ Recording Motor Functions of the Stomach,” “ New York Med. Jour.,” June 22, 1895, p. 772). We used an intragastric deg- lutable rubber bag (see illustrations, plate iv), which had small brass knobs extended at any desirable location, and when the bag was distended by blowing it up within the stomach the end elec- trodes pressed directly against the mucosa — usually one at the pylorus and one in the fundus ; the bag was in connection with a tambour or manometer recording on the Ludwig kymographion. We have already briefly stated that we were unable to produce any contraction of the human or animal stomach with the strongest currents to be obtained from one Grove cell prepared anew for each experiment, and the distance of the primary from the second- ary coil equal to zero when both electrodes were within the stom- ach touching the mucosa. We have elsewhere given our studies on the resistance which fresh human gastric mucosa offers to the constant current, and in the main can confirm Meltzer that percu- taneous and direct faradization of the stomach and intestines can produce no contraction of these parts. Not every current which, according to magnetic needles or the milliamperemeter, actually EFFECT OF ELECTRICITY ON GASTRIC PERISTALSIS. 305 penetrates the gastric wall causes contraction. For instance, with one electrode within the stomach of man or dog, and another on the gastrocnemius, the skeletal muscle may contract vigorously and the stomach remain passive. Again, in human subjects the factors of natural peristalsis occurring under the nervous tension due to the experiment, and of suggestion, can not be satisfactorily eliminated. In a recent publication Einhorn has attempted to disprove the experiments of Meltzer, but, as far as can be judged from the report of the former (in the “ Archiv f. Verdauungskrankheiten,” Bd. n, p. 454), the experiments were not conducted along the same lines nor with the same regard for physiological detail as those of Meltzer. Einhorn gives brief synopses of eighteen experiments, twelve of which were made with frogs, with which Meltzer did not work, and from the results of which conclusions regarding the mammalian stomach can not be safely drawn. Three animals were rabbits ; in these the stomach is always full of ingesta, unless starved. Two were rats; one only was a dog ; the latter was the animal with which Meltzer mainly worked. Nor is it evident that Einhorn’s results, as stated by him, contradict those of Meltzer in salient points. Taking, for instance, the last experiment with the dog, Einhorn made three kinds of stimulations with the double electrode : (i) on the serous (peritoneal) surface, near the fundus — contraction ; (2) on the peritoneal surface over the pylorus — strong contraction ; (3) opening of the stomach, — one electrode against the mucosa, the other on the peritoneal layer outside ; a weak current causes slight peristaltic contractions. Meltzer does not, in his original paper, deny any of these possibilities ; even the contraction of the third experiment was witnessed by him when the inner electrode on the mucosa was placed near the outer one on the serosa. But with bipolar internal stimulation — i. e., with both electrodes on the mucosa — even Ein- horn does not claim to have obtained any peristalsis of consider- able tonicity. We incline to the opinion that satisfactory evidence has not yet been furnished that internal electric stimulation can influ- ence secretion or motility either way. This conclusion has been reached after years of experimenting on both functions in the Bio- logical Laboratory of the Johns Hopkins University. In a recent reply to Einhorn’s criticism, Meltzer accepts the explanation of the former, concerning the difficulty of penetration of the electric current to the muscular layer (Boas’ “ Archiv f. \o 6 LAVAGE AND THE GASTRIC DOUCHE. Verdauungskrankh.,” Bd. hi, Heft 2, S. 133). This maybe caused, according to Einhorn, by the mucosa being a bad conductor as well as by its being a very good conductor — leading the current away from the point of contact. We have shown conclusively that the fresh normal human mucosa is a poor electric conductor. Einhorn, however, assumes that the mucosa conducts so well that the cur- rent does not reach the muscularis, because it moves in the direc- tion of least resistance — in the glandular layer itself. Tests made with the mucosa peeled off from the other layers of the stomach of a dog under narcosis, with the milliamperemeter in the circuit, show that the fresh mucosa is practically a non-conductor. Indications for the Employment of Electricity and Manner of Appli- cation. — Direct gastric faradization is recommended for dilatations due to relaxation of the musculature, but not to stenosis, whether these cases are associated with reduced secretion or not. Relaxa- tions of the cardia or pylorus are benefited by the faradic current. Sensory disorders (gastralgia) are successfully treated with direct galvanization. Rosenheim (loc. cit.) believes that the galvanic current is more effective in debility of the peristalsis. In all symptoms of sensory irritation he prefers the constant current also, but in secretory disturbances he has ceased to use electricity; and we agree with him that, in the latter class, more can be accomplished by medicated douches and adapted acid or alkaline and bitter tonic medicines than with electricity. Brock confirms the good effect of galvanism on the course of gastric neuroses (“ Therap. Monatshefte,” June, 1895), though he is not so enthusi- astic as Einhorn. According to Goldschmidt, there are no distinct differences between the effects of direct galvanization and direct faradization ; but nevertheless he recommends the former for the painful, the latter for the functional disturbances of the stomach. In contrast with those mentioned, von Ziemssen prefers the percutaneous to the direct intragastric application ; his reasons are not very convincing, in the light of Meltzer’s and Goldschmidt’s experiments. The electric brushing of the skin of the abdomen, breast, and back, urged by von Ziemssen, seems to be a great stimulus for nervous energy in neuropathic cases. In this country, Allen A. Jones (“ Med. Rec.,” June 13, 1891), Charles G. Stockton (“ Med. Rec.,” 1889, p. 530), and D. D. Stewart (“ Therap. Gazette,” 1893, p. 744) have published clinical obser- vations on the intragastric employment of electricity, and there HYDROPATHIC AND ORTHOPEDIC METHODS. 307 is a fairly uniform agreement that the class of gastric neuroses, particularly the sensory neuroses, nervous vomiting, and anorexia, are special indications for electricity in the form of the constant current, and that the direct intragastric method is to be preferred to the percutaneous. In simple atony and atonic dilatations (but not in those depend- ent upon pyloric obstruction) the preference is to be given to the direct faradic current. The manner of application is simple ; the anode is, as a rule, swallowed, and forms the intragastric pole. The cathode must have the shape of a conveniently broad and long, felt-covered plate (Fig. 30), which, after it is dipped in warm water, is placed for ten minutes on the epigastrium ; thereafter passed slowly up and down over the spinal column from the cervical to the sacral region. The meter should always be in the circuit, in case the galvanic current is used, and the strength of the current be about twenty-five milliamperes. The electric bath, or electricity applied when the body is immersed in a saline bath, has its advantages in gastric neu- roses. For more complete literature of the subject the reader is re- ferred to the writings of Kuss- maul (loc. cit.), Einhorn (loc. cit., and Einhorn, “ Berlin, klin. Wochenschr.,” 1891, No. 23; also “ Zeitschr. f. klin. Med.,” 1893, xxm, p. 369), and Goldschmidt (“ Deutsches Archiv f. klin. Med.,” Bd. xv, p. 295). The latter investigator worked under Moritz, whose capital experiments on the motility we have already abstracted. Goldschmidt concludes that the “ direct faradization and galvanization of the stomach (distance of primary from secondary coil = zero, duration fifteen to twenty-five minutes) has only an unimportant and inconstant influence on the peristalsis, and on secretion it has no influence whatever.” Hydrotherapeutic and Orthopedic Methods. — Hydriatic pro- cedures are much lauded by German and French gastro-enterolo- gists. Most of these methods can influence the stomach only indirectly and secondarily, and therefore are of greater utility in functional disturbances than in the organic gastric diseases. These 308 LAVAGE AND THE GASTRIC DOUCHE. methods may be divided into (i) general or systemic, (2) special or local hydrotherapic treatments. The method to employ depends more upon the state of general health and the condition of the ner- vous system than upon any local condition. Wherever hydriatic treatment becomes necessary, it is imperative to send the patient to some well-managed institution, as most of the procedures can not be executed at home. Among the methods most employed are the various local and general douches — viz., fan douche; cold, hot, graduated, Scotch, and French douches. Among these we have tried the Scotch douche most frequently in gastric myasthenia. It consists of a stream of moderate intensity directed against the epi- gastrium for three or four minutes. But during this time the tem- perature of the water is changed every ten or twenty seconds from 28° to 8° R., or vice versa; it is much lauded by von Ziemssen and Rosenthal (“ Magenneurosen,” etc., Wien, 1886). There are, besides, many kinds of fine sprays, and the sponge, sea-salt, pour, dash, shower, shallow, vapor, and sitz-baths ; also a variety of packs, fomentations, and compresses (see Baruch, “ Hydro- therapy ”). A local application which is very soothing in gas- tralgic affections is the so-called Priessnitz pack, which consists simply of a towel folded together to the size of six by ten inches, and dipped into hot or cold water, wrung out so that there is no dripping from it, and then applied to the epigastrium ; a layer of oiled silk or gutta-percha paper is laid over it and the whole is snugly secured and held in place by a broad flannel bandage passed around the body. As a matter of fact, most patients feel relieved and free from pain, but how the quieting effect is pro- duced is a matter of conjecture. In the treatment of gastric ulcer hot cataplasms are very service- able. We are in the habit of using spongiopiline dipped into hot water and applied to the epigastrium after the excess of water is pressed out. The orthopedic appliances used in the treatment of gastric diseases are often only imperfect substitutes for the more lasting effects of proper operations. They consist of contrivances to support the stomach in gastroptosis, or to keep up a floating kidney and prevent its interfering with the gastric or intestinal peristalsis. Where the abdominal muscles have become so relaxed that they seem to drag the viscera downward instead of supporting them, a condition found in obesity (Hangebauch = pendulous abdomen), the Landau abdominal corset, for both sexes, has proven of un- INDICATIONS FOR GASTRIC MASSAGE. 309 doubted usefulness in many cases in the author’s practice. Ab- dominal gymnastics are the most effective prophylaxis against these conditions. Gastric Massage. — Von Ziemssen (“ Ueber d. physik. Behandl. chronischer Magen- und Darmleiden,” Leipzig, 1888, p. 29) and Rosenheim (loc. cit ., p. 146) consider massage a very subordinate means of treatment for stomach diseases. Ewald (loc. cit.), Boas Fig. 31. — Massage of the Stomach in Dilatation or Gastroptosis.— (Penzoldt and Stintzing, “ Handbuch d. Therapie” etc.) (loc. cit.), and Riegel (loc. cit.), however, believe that there is some- thing of value in the treatment. The best study of gastric massage was published by Zabludowsky (“ Berlin, klin. Wochenschr.,” 1886, No. 26) and Cseri (“ Wien. med. Wochenschr.,” 1889). The technic of massage differs according to the object to be accomplished. If it is intended as a passive exercise to strengthen the musculature, it is best done on an empty stomach, in bed before breakfast. But if the massage is expected to assist in the expulsion of chyme, it 3io GASTRIC MASSAGE. should be undertaken three to four hours after the principal meals. Massage can not be properly performed except on the uncovered skin. Indications for massage are given in the disturbances of the motor function's, viz.: (i) Those depending on myasthenia or atony; (2) depending on a stenosis of moderate degree; (3) cases of reduced secretion and chronic gastritis; (4) gastroptosis or pro- lapse of the stomach ; and (5) certain cases of nervous inhibition of peristalsis. In cancer, ulcer, hematemesis, all acute inflamma- tions in or around the organ, in excessive dilatation, distention, or Fig. 32. — Massage for Improving Gastric Tonicity. — {Penzoldt and Stintzing, “ Handbuch d. Therapie etc.) contraction, and in all cases of intragastric putrefaction, massage is contraindicated. Massage of the stomach and colon is generally practised with a view to support and strengthen the expulsive power of these organs ; secondarily, its use may promote the nutrition of the mucosa and favor the resorption of infiltrations. The technic varies with the indication. For improving the muscular tone of the empty stomach the masseur places himself to the right of the patient, who must lie on his back with knees slightly flexed. First movement ( a ) : Insert the left hand slowly TECHNICS OF GASTRIC MASSAGE. 311 and gradually deeply under the left arch of the false ribs, under and past the edge. To increase the pressure, gently press the right hand firmly on the left. Second movement ( b ) : Now describe small circles with the hands thus arranged, progressing slowly from the pylorus to the fundus. Third movement (r) : Perform strong vibratory movements toward the depth with the finger-tips, white a and b are being executed. F'ourth movement (d ) : Knead the stomach between thumb and four fingers, and in conclusion execute stroking passes, with extended four fingers, from left to right. Fig. 33. — Massage of the Stomach and of the Colon. — ( Penzoldt and Stintzing , “ Handbuch d. Therapie etc.) Massage of the full stomach is undertaken with a view to mix its contents thoroughly or to aid in forcing them into the duodenum. Zabludowski (loc. cit.) advises the pressing of the stomach against the spinal column, dividing it into halves; by compressing the half nearest the pylorus, he widens the latter by wedging the chyme through it into the duodenum. This is justifiable only where it is sure that the chyme is comparatively fresh, and not in a state of putrefaction. The author has repeatedly experimented with Zabludowski’s method, and frequently failed. It is doubtful 312 GASTRIC MASSAGE. whether the contents of very dilated stomachs can be expressed into the duodenum by massage. Combination of Massage and Medicated Irrigations of Stomach and Colon. — When solutions of chemicals are poured into the stomach or swallowed, they exert a more prompt and lasting effect if the organ is subjected to gentle massage during the time these solutions are in it. In case there has been retention of ingesta and processes of putrefaction, the stomach must first be thoroughly cleansed by lavage. If the solutions contained active chemicals they must be removed after the massage by careful irri- gation with plain water. This treatment is indicated in hyperacidity with alkaline solutions, in sub- or anacidity with diluted HC 1 and all conditions of chronic hyperemia, excepting the active processes given above as contra- indications. In states of relaxation of muscular tonus and in hyperesthesia and gastralgia we have observed most gratifying improvement where other methods had proved futile. The technics of the method are simple : in some cases the patient may be permitted to drink the medicated solutions, but it will gener- ally be preferable to pour them in through the tube, especially when lavage is indicated before the procedure. The taste of some of the drugs that are necessary, prevents drinking the solutions, or it may be requisite that the mouth or esophagus be protected from the agents. As soon as the solution is in the stomach, the patient occupying the dorsal recumbent position, with the knees flexed, the masseur begins with gentle but deeply penetrating compression of the epigastrium and hypogastrium with palmar surface of the fingers. Thereupon stroking of the stomach region from above downward ; from left to right, and reversely ; next follow circular friction move- ments of the stomach especially, but also over the entire abdomen. During the massage the dorsal position should be exchanged with the right and left lateral position. The medicines inside the organ will in this manner be extensively and thoroughly brought in con- tact with the gastric walls, and it is conceivable that, through the increased circulation effected thereby, absorption is favored in a manner not otherwise obtainable. The duration of this method should not exceed ten minutes with indifferent substances, and only five minutes if chemicals with a decided effect are used. The agents that have been employed are the following : In anacidity and achylia , HC 1 2 : 1000; also normal salt solutions and one per cent, of ichthyol. In anorexia , solutions of the tinctures of Colombo, MINERAL SPRINGS. 3 I 3 calisaya, quassia, gentian, and hops. In hyperacidity , the natural alkaline mineral waters, such as Saratoga Vichy, or per cent, solution of Carlsbad salts. Jaworski’s antacid solution is useful here, and also suspensions of bismuth and solutions of nitrate of silver i : 1000. In hypersecretion the same solutions as in hyper- acidity are applicable ; but in addition to these we have employed tannigen, four grams to one liter, rendered soluble by bicarbonate of sodium. The substances applicable in gastric fermentation have been recorded in the chapter on Motor Insufficiency. CHAPTER V. MINERAL SPRINGS. The Uses and Abuses of Natural Mineral Waters in Diseases of the Digestive Orga ns . * With such a wealth of valuable mineral springs in this country it is difficult to understand the large annual exodus of Americans to foreign water resorts. We fear the fault rests with the Ameri- can physician, not the American waters. Few native physicians give to the selection and adaptation of proper mineral waters the consideration it deserves; whereas in German, French, and English practice this forms a common and important factor. Ac- cording to Baruch, even American doctors resident at the springs do not insist upon precision in proper drinking, diet, hydrotherapy, or exercise. The surpassing virtues of our American mineral waters can be attested only by making an individualizing selection of the waters for each case, after establishing the diagnosis. Too much empiricism, too much fashion and sport, too much alcohol, and not sufficient peace and quiet of mind exhibit them- selves at our American springs. Without a diagnosis — not to speak of test-meals — we have known * In the preparation of this chapter we have availed ourselves of the Analyses of the Mineral Springs of the United States as given in the records of the Department of the Interior (Agriculture), Washington, D. C. ; and in the description of the physiological effects of the various springs we have followed the works of Flechsig, S. Baruch, Lud- wig, and G. Thompson in reference to waters with which we have no personal experience. 21 « 3H MINERAL SPRINGS. of numerous instances where the waters of springs were ordered. Systematic mineral-water treatment should be recommended only after the institution of careful chemical and physical examinations. In reference to the abuse of mineral waters, we limit our- selves to their misuse in gastric diseases. We would exclude, first, all cases of motor insufficiency of any kind, whether of the simple atonic or the stenotic form, whether with pronounced dilata- tion or not, because we know that water is not absorbed from the stomach, and hence can only aggravate (by its weight) the myasthenia and dilatation. Where, however, the various saline and alkaline waters can be readily obtained, they serve admirably for lavage. The sodium chlorid spring-water is beneficial in sub- or anacidity, and the alkaline waters whenever hyperchylia is associated with dilatation. In neoplasms of the stomach, particularly in carcinoma, mineral- water treatment is harmful. For ulcer, the Carlsbad springs have been much lauded by Leube and others; but we coincide with Ewald in the opinion that the same or perhaps more rapid effects would have been obtained in such cases, had patients taken the rest cure at home. Rest, diet, and effective local treatment are the things most needed, and these can be obtained much more readily at home than elsewhere. For, after all, as far as gastric sufferers are concerned, the most important things, even at the springs, are rest to body and stomach in particular, diet, suitable food, good cooking, etc. In acute gastritis mineral waters are useless. There remain still to be considered the neuroses of secretion and motility. All secre- tory neuroses are, more or less, indications for mineral-water treat- ment, particularly those in which an excessive amount of HC1 is formed, with which the alkaline waters combine, at the same time exerting a very desirable astringent effect on the mucosa; for these, such waters as the Saratoga Vichy are applicable. In achylia of nervous origin the saline waters might rationally be tried ; but where the glandular elements are destroyed they can not restore the secretion, although they may aid in dissolving mucus and keep- ing the membrane cleaner than otherwise. In the motor neuroses, if dependent upon hyperchylia or hypersecretion, the alkaline waters may benefit by removing the causes, as stated above ; but in insufficiency of the pylorus and cardia we have neither heard of nor seen improvement. The proper field for these waters is undoubtedly chronic gas- INDICATIONS FOR THE USE OF MINERAL WATERS. 315 tritis. With their judicious use much good can be effected. It should not be overlooked, however, that there may be a chronic gastritis with normal or excessive acidity ; here the alkaline waters are to be preferred to the salines. In chronic gastritis with achylia only salines of mild concentration are useful; for the powerful saline (NaCl) waters, such as Carlsbad (Miihlbrunnen), may un- doubtedly cause an injurious, alkaline, irritative transudate from the mucosa if retained in the stomach. In chronic gastritis the still or the carbonated saline waters undoubtedly are beneficial, by their stimulating effect on the secre- tions. Gastric sufferers should drink their spring-water preferably warm. Cold spring-water should be rendered tepid by the addition of warmed water from the same spring. All waters which are to act on the stomach are tolerated better warm than cold. In uncomplicated hyperacidity and hypersecretion the alkaline or the mixed alkaline saline springs are beneficial. In this country the Saratoga Vichy is the most available. Alkaline waters also benefit peptic ulcer cases when there have been no hemorrhages for some time, because they neutralize the acid excess and actually lessen the activity of secretion. Waters containing sodium sul- phate are applicable to the treatment of secondary gastritis. According to Stille and Maisch there are, indeed, two classes of patients who require the use of very different mineral waters. The first is composed of that large body of invalids in whom there exists no organic change of structure, but whose functions are merely weakened or clogged by the strain of business, the exhaustion of pleasure, excesses in eating or drinking, or, in this country especially, by the manifold errors committed in the preparation and consumption of food and the disregard of hygienic rules in their habits of living. The second consists of that smaller but still numerous class of persons who, besides being more or less injured by the causes of ill health just enumerated, have been affected with definite diseases, and especially rheumatism, gout, calculous disorders, cutaneous eruptions, scrofula, syphilis, dia- betes, paralysis, uterine disorders, etc. Of these two classes the former is benefited most by a visit to the less mineralized springs, while the latter requires a course of active medicinal treatment such as the stronger mineral waters afford. In both classes of patients, but particularly in the first, the action of the waters is only one out of many influences that combine to restore their health. Toward that end a total change of habits is one of the 3 j 6 MINERAL SPRINGS. most influential agencies in very many cases. Escape from the anxieties and fatigue of business, from the excitement of fashion- able life, the mental tension of political and professional pursuits, the worrying annoyances of domestic affairs, endured, perhaps, in a large city, with all its enervating social duties, its Babel-like sounds, and its polluted atmosphere, — escape from these alone ought to suffice to restore the disturbed balance of health. When we consider how much more probable must this result become when fatigue, anxiety, contention, wearisome routine, and foul air are exchanged for repose and peace in the midst of novel scenes and new associates, and freedom from the onerous conventionali- ties of fashionable life, different apartments, food, and occupation, it may even seem doubtful whether, after all, some other new resi- dence would not profit the invalid as much as the frequented springs. But there are two reasons against this conclusion : the one is that, with many persons, relief would be impossible without an exercise of the faith which gives potency to waters as well as to other remedial agents; and the other is that even the purest of these waters, systematically used, especially in conjunction with bathing and regular exercise, do, in a greater or less degree, depu- rate the system through the kidneys, bowels, and skin, and by a gentle but sustained action gradually remove effete products of tissue-change from the system and free the organs from the poisons that tainted them. Judiciously used under the advice of a competent physician, these almost neutral waters and the milder saline springs are capable, in a few weeks, of changing the languid, indifferent, pale, and feeble invalid into the lively and energetic leader of the gay crowd. Such rapid transformations are frequently witnessed, especially at the hot springs of Virginia, the Bedford springs, Pa., at some of the Saratoga springs (though in the last- mentioned place routine hygienic treatment becomes more difficult because of numerous side temptations), and certain European springs, such as Wildbad, Gastein, and Pfeffers, none of which contains any considerable proportion of mineral ingredients. But these waters, whether drunk warm or cold, if they are largely used, act as organic purgatives, and increase materially the total amounts of solids, and especially of urea, excreted with the urine, without causing the debility which an equal discharge from the bowels would occasion. Alkaline Waters. — The chief ingredients of these waters are the alkaline carbonates, especially the carbonate of sodium. They ALKALINE WATERS. 3*7 also contain varying amounts of the carbonates of lime, mag- nesium, lithium, sodium chlorid, etc., and many of them are strongly charged with carbonic acid gas. Although it is probable that the other saline constituents may contribute to the total phys- iological effects of these waters, they owe their main therapeutic activity to the alkaline salts they contain. The temperature of these springs is also a point worthy of consideration. In a general way it may be said that the physiological action of these waters is like that of any alkaline salt, plus the effect produced by the circu- lation of large quantities of water in the system. The carbonate of sodium neutralizes free acids or fermentation products in the stomach, whether taken during or after meals. According to Brunton and Sidney Ringer, the stronger alkaline waters, if taken before meals, increase the secretion of gastric juice. This, in the author’s experience, is doubtful. The fact is, distilled water will also cause a secretion of gastric juice in the normal stomach, but will not neutralize the acid thus secreted, as the alkaline waters must invariably do. This, however, is not an effective way of treating anacidity. For this condition the treatment is given in the clinical part. The carbonic acid set free by the decomposi- tion of the carbonates in the stomach and the sodium chlorid usually present in these waters act as a stimulant to the gastric mucous membrane, promoting secretion and counteracting any disturbing influence exerted by the carbonate. The free carbonic acid frequently contained in waters of this class, by its stimulating effects on gastric peristalsis, accelerates digestion, and thereby increases the desire for food. It would appear, therefore, that the alkaline waters have a wide range of usefulness. They seem to be especially indicated in gastric affections in which there is an excessive production of hydrochloric acid, as in acid dyspepsia, atony of the gastric mucous membrane, and gastric ulcer. In all catarrhal conditions of the stomach they are most serviceable, but a free and prolonged use lowers the nutrition, except in case of waters containing chlorid of sodium. The names of a few of the more important Alkaline Waters are here appended : Vichy, in France; Ems and Fachingen, in Germany; Saratoga Vichy (rich in C0 2 ), New York; St. Louis Springs, Michigan (poor in C0 2 ); Bethesda Springs, Wisconsin. Other sodium chlorid waters, containing also some carbonates and C0 2 , are: MINERAL SPRINGS. Hathorn, Congress, and Kissengen Springs, in Saratoga, New York ; Homburg, Wiesbaden, Kissingen, and Selters, in Germany; Bour- bonne, in France. All alkaline waters contain more or less carbon dioxid, and their most important ingredients are the alkaline carbonates. They also contain sodium chlorid and sometimes sodium sulphate. In some, one variety of salts, in others, another preponderates. Gen- erally speaking, the European waters are richer in alkalies than are the American. Alkaline waters are useful in uric acid diathesis and lithemic conditions, gout, chronic rheumatism, obesity, hepatic engorgement, gall-stones, hyperacidity, gastric ulcer, and catarrhs of the mucous membranes, especially of the stomach, respiratory tract, and bladder. Alkaline Sulphur Waters. — Richfield Springs, Sharon Springs, and Avon Springs, in New York; Greenbrier White Sulphur Springs, in West Virginia; Harrogate, in England; Neuendorf and Meinberg, in Germany; Aix-la-Chapelle, in Rhenish Prussia. Those waters containing sulphureted hydrogen in addition to other ingredients are used moderately in gout, chronic rheumatism, obesity, and chronic eczema. They are often supplemented by a course of chalybeate waters. Alkaline and saline purges contain a high percentage of sodium and magnesium sulphates. These waters are often called “ bitter waters.” Such are Piillna, in Bohemia (the strongest of all and one of the oldest known) ; Carlsbad (Sprudel), in Bohemia ; Marien- bad (Kreuzbrunnen), in Bohemia; Friedrichshall, in Germany; Franz Josef, in Austria; Kissingen Bitter Water, in Bavaria ; Hun- yadi Janos, in Hungary; Rubinat Condal Spring and Villacabras, in Spain ; Crab Orchard and Estill Springs, in Kentucky ; Bedford Springs, in Pennsylvania ; Epsom, in England ; some of the Sara- toga waters. These waters are useful to counteract indiscretions in diet and congestion of the liver. The Rubinat water is effective and possesses the advantage of being less disagreeable than many of the others. Villacabras water is a Spanish sodium sulphate, strongly purgative water, obtained not far from Madrid. These waters should be taken either very cold or in a half-pint of very hot water. If drunk lukewarm, their taste is nauseous and may excite emesis. We advise that these powerful waters be entirely avoided where there is any distinct organic disease of the stomach. SALINE WATERS. 319 Various other zvaters are the Alum Springs, in Virginia ; Oak Orchard Acid Spring, in New York; Bourboule, in France, which contains arsenic. Roncegno water is a ferruginous arsenical water from the Tyrolean province of Trent. COMPARATIVE CHART ILLUSTRATIVE OF ALKALINE WATERS.— [Baruch.) One Pint Contains : American. European. Sodium Carbonate. Carbonic Acid Gas. Temperature. Other Prominent Constituents. Vichy (Grand Grible Spring) , Grs. Cub. in. Fahr. Ojo Caliente Spring, France, .... 26 14 105.8° Sodium chlorid, 4 grs.; sodium sulphate, 2 grs. ; potassium car- bonate, 2 grs. Sodium chlorid, 4 grs.; sodium sulphate, 1 gr. New Mexico, . . Fachingen Spring, 14 IOO° Saratoga Vichy Germany, . . . 19 32 50° Sodium chlorid, 4 grs.; calcium carbonate, 2 grs. Spring, New Y ork, Ems (Kesselbrun- nen Spring), II 48 5 o° Calcium and magnesium carbonates, 17 grs.; sodium and potassium chlorids, 18 grs. St. Louis Spring, Germany, . . . IO 6 115 0 Sodium chlorid, 7 grs.; calcium carbonate, 1 gr \ Michigan, . . . 7 1 5 o° Calcium and magnesium carbonates, 6 grs.; calcium sulphate, 7 grs. Saline Waters. — This class may be conveniently subdivided into, first, waters containing chiefly the chlorid of sodium; and, second, waters containing large quantities of the sulphates of sodium and magnesium — the so-called “bitter waters” of German authors. The Sodium Chlorid Waters. — These waters contain, besides large quantities of sodium chlorid, a certain proportion of other chlorids, especially those of lime and magnesium, and small amounts of alkaline and earthy sulphates and carbonates, iodids 320 MINERAL SPRINGS. and bromids. Carbonate of iron is sometimes present in consid- erable quantity. The gases consist for the most part of carbonic acid, which renders the water more agreeable to the palate and more readily absorbed. Some of these waters are heavily charged with sulphureted hydrogen. They occur both as cold and ther- mal springs, and may be utilized both for drinking and bathing purposes. The physiological action of these waters is chiefly attributable to the presence of sodium chlorid. This salt, as is well known, has a stimulating effect upon all the mucous membranes of the body, especially that of the gastro-intestinal tract. In the stomach it dis- solves the mucus, increases the secretion of gastric juice, thereby promotes the digestion of albuminous substances, and excites peris- talsis. In the intestines it stimulates the flow of pancreatic juice and bile, and, owing to its well-known influence on the process of osmosis, promotes the absorption of food. Intestinal peristalsis is also increased, and, if the sodium chlorid is present in large quan- tity, the water may, in its effects, be laxative and even purgative. Some authors have regarded this purgative action as representing the chief therapeutic virtues of these waters, but, according to Flechsig, it is subordinate in importance to the effect of the sodium chlorid on the blood. He states that this salt exerts considerable influence on the process of tissue metabolism, augmenting the metamorphosis of nitrogenous matters and increasing the oxida- tion of albuminous substances, as is shown by the increased quan- tity of solids in the urine. The iodids and bromids contained in some of these waters are usually present in such very minute amounts that it is doubtful whether they contribute to their thera- peutic action ; at any rate, it is impossible to separate their effects from those of the sodium chlorid. The therapeutic indications of sodium chlorid waters, as based upon their physiological action, are sufficiently obvious. Their stimulating effects upon the mucous membranes have been utilized in the treatment of catarrhal processes, especially in the stomach, duodenum, and bile-ducts; and in chronic intestinal catarrh associated with constipation, their use has been highly com- mended. BITTER OK PURGATIVE WATERS. 321 COMPARATIVE CHART ILLUSTRATIVE OF SALINE WATERS.— [Baruch.) American. European. Sodium Chlorid. Carbonic Acid Gas. )nk Pin* it E = H r Contains: Other Prominent Constituents. Homburg (Eliza- bethbrunnen), Grs. Cub. in. Fahr. Grains. Ballston Artesian Lithia Well, New Germany, . . . 79 48 50° Chlorids of calcium and. magnesium, 15 ; cal- cium carbonate, 11. York, Wiesbaden (Koch- brunnen), Ger- 93 53 Magnesium and calcium carbonate, 34 ; potas- sium chlorid, 4; lithium carbonate, 0.7. Hathorn Spring, many, .... 52 17 155 ° Chlorid of potassium, 1 ; calcium carbonate, 3. Saratoga, New York, Bourbonne (Fon- taine Chaude), 64 47 47 ° Calcium and magnesium carbonates, 28. Congress Spring, France, .... 46 149 0 Calcium chlorid, 5 ; cal- cium sulphate, 6. Saratoga, New York, Kissingen (Rak- 50 49 52 ° Calcium and magnesium carbonates, 21 ; sodium bromid, 1. 06. Kissengen Spring, oczi), Germany, 44 42 51° Potassium chlorid, 2 ; calcium carbonate, 8. Saratoga, New York, 42 45 0 0 Calcium and magnesium carbonates, 26 ; sodium carbonate, 8 ; lithium carbonate, 0.64. Selters, Germany, 17 30 62° Sodium carbonate, 6. Saratoga Seltzer Sodium carbonate, 2; cal- cium and mignesium carbonates, 10. Spring, New York, 17 5 o° Bitter or Purgative Waters. — This name has been applied to waters characterized by a high percentage of the sulphates of sodium and magnesium. They also contain considerable quanti- ties of the sulphates of lime, and the carbonates of lime and magnesium, though rarely small amounts of carbonic acid gas. Carbonate of sodium, however, is seldom, if ever, found in them. The chief physiological action of these waters is comprised in the stimulating effect which they exert upon the mucous mem- branes of the gastro-intestinal tract. They give rise to a profuse 3 22 MINERAL SPRINGS. watery secretion of a serous, or even mucous, character, and thus act as purgatives. If taken in large quantities, they frequently produce gastric and intestinal disturbances, and their protracted use is apt to be followed by atony of the intestines and intestinal catarrh. It is as yet a matter of speculation whether this purga- COMPARATIVE CHART ILLUSTRATIVE OF BITTER AND PURGATIVE WATERS. — {Baruch.') One Pint Contains: American. European. Sodium Sulphate. Magnesium Sulphate. Carbonic Acid Gas. Temperature. Other Prominent Constituents. Grs. Grs. Cub. in. Fahr. Crab Orchard, Foley's Spring, Piilln a, Bohemia, 124 93 Chlorid of magne- sium, 16 grs.; mag- nesium carbonate, 6 grs. Kentucky, . . Friedrichshall, 7 25 Calcic carbonate, 7 grs. ; potassium sul- phate, 1 gr. Estill’s Springs, Irvine Springs, Germany, . . 41 39 5 46° Sodium chlorid, 67 grs.; magnesium chlorid, 31 grs.; calcic sulphate, II grs. Kentucky, . . Carlsbad (Spru- 32 Calcic carbonate, 4 grs.; sodium chlo- rid, 2 grs. Bedford Springs, del), Bohemia, 19 8 162° Sodium carbonate, 9 grs.; sodium chlo- rid, 8 grs. Pennsylvania, Marienbad (Kreutzbrunnen) , 10 9 58° Chlorid of sodium, I gr. ; calcium sul- phate, 2 grs. Harrodsburg Spring, Saloon Spring, Ken- Bohemia, . . 36 15 53 ° Sodium carbonate, 8 grs.; sodium chlo- rid, II grs. tucky, .... 28 Calcic sulphate, 10 grs.; sodium chlo- rid, I gr. tive action is due to the increased exudation of fluids, or whether it results from the stimulation of intestinal peristalsis, as is assumed by Flechsig and others. Owing to the increased peristalsis, the passage of food through the intestines is accelerated ; and in con- sequence of the diminished absorption of nutriments engendered SULPHURETED WATERS. 323 by this, a loss of weight and disappearance of the fatty tissue results. It follows from the above considerations that the use of these waters is restricted to cases in which we desire to stimulate the intestinal secretions, as in chronic constipation occurring in ple- thoric persons, engorgements of the abdominal and pelvic viscera, hemorrhoids, etc. They also prove serviceable in cases of obesity, as part of a treatment of denutrition. On the other hand, their use is contraindicated in anemic persons, and where there is great irritability of the stomach and intestines, with a tendency to diarrhea. American waters of this class are somewhat weaker in sulphates of sodium and magnesium than the European, but the quantity of purgative salts present in the former is quite sufficient to produce active therapeutic effects. All these waters contain a considerable amount of sodium chlorid, which contributes essentially to their physiological action. The Bedford Spring (Pa.) water is especially to be recommended on account of its mildness. It is, in our opinion, of no advantage when spring-waters possess an excessively large percentage of drastic salts. In a concentrated solution magnesium chlorid acts as a cellular poison on the superficial gastric and intestinal epithe- lium when used for weeks. Bedford Mineral Magnesia Spring has also a mildly diuretic effect; its laxative effect is not experienced until at least 500 c.c. are taken in twelve hours. Sulphureted Waters. — The constituent imparting to these waters their distinguishing characteristic is the sulphureted hydro- gen which they contain in greater or lesser amount. With this gas we find associated a varying quantity of sulphur combinations, such as the sulphids of potassium, sodium, calcium, and magne- ’ sium. They also contain the alkaline and earthy sulphates and carbonates, the chlorid of sodium, and the sulphates and carbonates of iron ; and these are frequently present in large quantities, and certainly play a not unimportant part in the therapeutic action of these waters. According to Daland, “ a sulphur spring of moderate strength contains not less than twelve cubic inches of sulphureted hydrogen in the gallon, though many springs contain so small an amount that therapeutically they are inert, and the good effects observed are due to the influence of the increased use of water, change of scene and climate, cessation of work, regular meals, good hygiene, and hope — all of which contribute strongly to restore 324 MINERAL SPRINGS. health at all springs.” Many of the sulphur waters are thermal, and are chiefly employed in baths. Regarding the physiological action of sulphur waters on the system, nothing positive can be said. Various plausible theories have been proposed to account for their curative effects in the diseases for which they are employed. It is claimed that their chief action is exerted on the intestinal canal, where they stimulate the functions of the glands, augmenting secretion and producing laxative effects. When administered for prolonged periods they give rise to gastro-intestinal disorders and exert a debilitating influence upon the blood, heart, and lungs, as evidenced by anemia, cardiac weakness, etc. According to Leichtenstern, the sulphureted hydrogen absorbed into the blood is rapidly converted into sul- phuric acid, and is therefore devoid of any specific effect, unless present in very large amounts. On the other hand, Stifft concludes that the sulphureted hydrogen has a specific excitant action upon the sensitive fibers of the pulmonary branches of the pneumogas- tric and upon the respiratory, cardiac, and vasomotor centers, its prolonged use giving rise to paralysis from overstimulation. In this way he explains the action of the sulphur waters upon the respiratory and circulatory systems, upon tissue-metabolism, and upon the secretory and excretory functions. These waters have been administered internally in passive con- gestion of the abdominal and pelvic viscera, especially in plethoric persons ; in enlargements of the liver and spleen ; hemorrhoids ; chronic intestinal catarrh; and chronic poisoning by metals. In the form of baths they have been recommended in gout and chronic rheumatism, but their curative effect in these cases is attributable to the elevated temperature of the waters rather than to any specific action of the sulphureted hydrogen or other constituents. At many baths the internal or local use of the waters is combined with inhalation of the gases or of the nebulized waters ; and this method has been found useful in the treatment of chronic catarrhs of the pharynx, larynx, and bronchi. Sulphureted waters are, in our estimation, worthless as a therapeutic agent in gastro-intestinal diseases. Sulphureted waters are abundantly represented in the United States. In Virginia they are particularly well represented — vide Jordan’s White Sulphur Springs, Frederick County ; Greenbrier White Sulphur Springs, Roanoke Red Sulphur Springs, Yellow Sulphur Springs, Montgomery County, Va., and many others in CHALYBEATE WATERS. 325 other States. There is certainly no necessity for traveling to Aachen-Baden (near Vienna), Leuk, or Weilbach to use waters of this type. The following chart illustrates the superiority of the sulphur waters of America : COMPARATIVE CHART ILLUSTRATIVE OF SULPHURETED WATERS. — {Baruch.) One Pint Contains: American. European. Sulphureted Hydrogen. Sulphids. Temperature. Other Prominent Constituents. Cub. in. Grs. Fahr. Sandwich Spring, On- Neundorf, Germany, i.:8 o -55 53 ° Calcium and magnesium sulphates. 10 grs. tario, Canada, . . Aix-le-Bains, 5 2° Chlorid of magnesium, 19 grs.; calcium sulphate, 15 grs. France, 0.82 108 0 Calcium carbonate, 1 gr. Sharon Spring. White Sulphur Spring, New York, . . . Harrogate, Eng- 0 28 00 0 Calcium and magnesium sulphates, 24 grs. Paroquet Spring, land, 053 1-54 Sodium chlorid, 86 grs.; potassium and magne- sium chlorids, 10 grs. Kentucky, . . . 3 75 Sodium chlorid, 39 grs. Meinberg, Germany, 0.61 0 67 00 0 Sodium sulphate, 6 grs. Salt Sulphur Spring, Iodin Spring, W. Virginia, .... Sodium sulphate, 3 grs.; calcium sulphate, 8 grs. Chalybeate Waters. — A large number of mineral springs con- tain the salts of iron, but the quantity present is frequently so small as to be practically devoid of therapeutic effects. In the class under consideration only waters containing a sufficient quan- tity of chalybeates to be of value in the treatment of disease will be mentioned. Iron salts usually occur in the form of the carbonate or sulphate. Other constituents, which are sometimes present in large amounts, are the alkaline carbonates and sulphates, the earthy carbonates, sodium chlorid, alum, and sulphuric acid. Alum often exists in considerable quantities, especially in the chalybeate springs of Virginia. 326 MINERAL SPRINGS. Chalybeate waters containing the carbonate of iron are clear, odorless, have a slight inky taste, and are highly charged with carbonic acid gas, which renders them palatable. They are chiefly employed for drinking purposes. The sulphate-of-iron waters have a marked astringent taste, which sometimes proves an objec- tion to their use. This astringency may be decidedly increased by the presence of alum. The following chart* illustrates the superior quality of some American chalybeate springs : CHALYBEATE WATERS. — [Baruch. ) One Pint Contains: American. European. Sulphates of Iron. Carbonates of Iron. Carbonic Acid Gas. Other Prominent Constituents. Brighton, England, I 80 Calcium sulphate, 4 grs. Church Hill Alum Springs, Virginia, Spa (Buhon), Bel- 19 8 Magnesium and calcium sulphates, 22 grs. ; alu- minium sulphate, 9 grs. gium, 0.67 71.6 Small amounts of calcium carbonate and alumina. Rock Enon Springs, Virginia, .... Schwalbach (Stahl- brunnen), Ger- 1.78 Calcium and magnesium sulphates, 2 grs. ; cal- cium and sodium carbon- ates, alumina. Vichy Springs, New many, 50.2 Calcium carbonate, I gr. ; manganese carbonate 0. 10 gr. Almaden, Cal., . St. Moritz (Grande Source), Switzer- O.60 29.8 Sodium carbonate, 17 grs.; calcium carbonate, 3 grs ; magnesium sulphate, I gr.; sodium chlorid, 4 grs. land, 39 2 Sodium carbonate, 1 gr.; calcium carbonate, 6 grs.; sodium sulphate, 1 gr. Estill Springs, Ken- tucky, 4-15 Calcium carbonate, I gr.; magnesium sulphate, I g r - * These charts make no claim to completeness. Boas has suggested a more extensive enumeration of the German chalybeate springs in this book (see Review on Hemmeter’s “ Diseases of the Stomach,” “ Deutsche med. Wochenschrift,” April 14, 1898, No. 15 ; * ‘ Literaturbeilage,” No. 10, p. 58). This, however, can not fairly be considered INDICATIONS FOR THE USE OF ACIDULOUS WATERS. 327 The physiological action of chalybeate waters is essentially similar to that of all iron compounds; they promote constructive metamorphosis, increasing the number of red corpuscles in the blood and stimulating all the body-functions. For internal use the waters containing the carbonate of iron are preferable, since they are less apt to disturb the stomach, and are more easily assimilated, owing to the carbonic acid gas present. According to the character of the case, it may be necessary to select an iron water containing alkalies, sodium chlorid, sulphate of sodium and magnesia, or alum. The chalybeate waters have been recommended in anemia, chlorosis, and all conditions attended with anemia, such as hysteria and neurasthenia ; chronic endometritis, dysmenorrhea, amenorrhea, chronic gonorrhea, and spermatorrhea; chronic affections of the kidneys, diabetes mellitus, chronic gastritis, nervous dyspepsia, chronic diarrhea, etc. Among the iron and alum springs, Bedford Alum Spring has been found remarkably efficacious by Baruch in chronic diarrhea, which had resisted both private and hospital treatment. The contraindications to their use, as given by Flechsig, com- prise all febrile and congestive conditions and advanced organic diseases of the lungs, liver, and kidneys. The sulphate-of-iron waters are excellent astringents and disinfectants, and have been highly recommended in chronic diarrhea, gastric ulcer, etc. Acidulous Waters. — These waters owe their therapeutic prop- erties to the large quantity of carbonic acid gas they contain, the solid constituents being present only in small amounts. As has been stated, many alkaline and saline waters contain considerable quantities of C0 2 ; but its effects, whatever they may be, are com- pletely subdued by those of the mineral ingredients. In the acid- ulous waters, however, the carbon dioxid is the chief therapeutic agent, and for this reason it becomes necessary to discuss them as a separate class of mineral waters. The physiological action of carbonated waters is comprised in a gentle stimulative effect upon the mucous membrane of the stomach, promoting peristalsis, and thereby a more rapid evacua- tion of its contents. The pulse and respiration are said to be within the range of our work. We can not even do justice to our native mineral springs. For fuller information we must refer to the works quoted in the beginning of this chapter. 328 IMPORTANT MEDICINAL AGENTS IN GASTRIC THERAPY. slightly accelerated, and a large quantity of urine is excreted. It seems, however, that this diuretic effect is not attributable to the carbonic acid gas, as is assumed by some authors, but rather to the large quantities of water which the patient is able to imbibe with- out distress, for the quantity of the gas absorbed into the blood through the walls of the stomach is certainly too small to produce systemic effects. The acidulous waters have been chiefly recommended in gastric disorders, especially those of neurotic origin; and, owing to their agreeable taste, they form excellent table waters. They relieve nausea, increase the appetite, and aid digestion by stimulating the secretion of HC1. On account of their stimulating effect upon the peripheral cutaneous nervous system, they have also been employed as baths. CHAPTER VI. IMPORTANT MEDICINAL AGENTS IN GASTRIC THERAPY. HC1 is given in the absence or diminution of the normal secre- tion mainly for three purposes : (1) To supplement gastric prote- olysis ; (2) to act as an antiseptic; (3) as a tonic and stomachic. To these effects, that we have in mind in supplying PI Cl, may be added its influence as a regulator of the gastric peristalsis ; and that it brings the insoluble calcium and magnesium salts of the ingesta into solution ; in fact, all of the objects and functions that are recognized as physiological to the HC1 (see p. 49) may be at least partially accomplished by supplying it in sufficient quantity. The HC1 deficit — i. e ., the amount of decinormal HC1 solution that must be added until the reaction of the chyme shows free HC1 — should be determined when the reactions for free HC1 turn out negative. In one case the deficit may be very slight, in another very considerable. Slight deficits generally yield readily to treatment by diet and lavage, often without adminis- tration of HC1 ; large deficits may be a sign of atrophy and never yield to HC1 therapy, no matter how much is given. But the question arises, Can it be supplied in sufficient quantity ? The simple presence of free HC1 does not contraindicate the LOSS OF HCl SECRETION DISPOSES TO ILL HEALTH. 329 administration of the acid. Positive reaction to Congo paper and phloroglucin-vanillin indicates, it is true, that MCI is secreted in excess of what is required to combine with the food. In healthy digestion it is always found that this excess amounts on the average to 30 c.c. of a decinormal solution of NaOH after an Ewald test-meal (in Baltimore) ; and it seems to be what is necessary or advantageous, not for digestive purposes (for even with a large excess of HCl it is not the rule for all the proteid matter to be digested in the stomach), but for destroying the exuberance of micro-organisms swallowed with the food. The frequently quoted cases without any gastric secretion whatever who succeed in maintaining their nitrogen equilibrium, — and we have seen many such, — and the experiment with the dog (Kaiser and Czerny) whose weight was kept up although the largest portion of the stomach was removed, and the total extirpations of the stomach by Schlatter, Brigham, and others, constitute but a weak argu- ment against the therapy of HCl. For although such patients manage to get along fairly well, it is only under the most careful diet and by taking very little exercise that they maintain their health. Permanent and perfect health with total absence of gastric secretion is rarely observed, except in those who are able to rest much and have their food prepared with great care. These facts must not be overlooked in the work of von Noorden (“ Ueber die Ausnutzung der Nahrung bei Magenkranken,” “ Zeitschrift f. klin. Med.,” 1890, Bd. xvii), which demonstrated that absolute and per- manent deficiency of gastric juice may be accompanied by perfect health. This health is perfect under the conditions mentioned, but when they are taxed by work or the diet is not the usual one, suffer- ing becomes manifest. If achylia gastrica could really exist without any subjective or objective disturbance, how is it that so many of these patients consult the stomach specialists and are reported by them in literature? When we must work for our living and can not have the benefit of the dietetic kitchen at all times, we must have an active gastric juice to partially, at least, disinfect and dissolve our food, and a person who secretes no gastric juice is or soon becomes a patient. In a recent article on Achylia Gastrica by F. Martius and O. Lubarsch (published by T. Deuticke, Leipzig, 1897), the authors arrive at the conclusion that neither simple achylia nor that depen- dent upon atrophy of the mucosa (anadenia) can bring about severe anemic or cachectic conditions unless motor insufficiency, atrophy of the intestinal mucosa, or general diseases (tuberculosis, lues, 22 330 IMPORTANT MEDICINAL AGENTS IN GASTRIC THERAPY. infections, etc.) are added. Even if this is true, generally speaking it does not disprove the statement that absence of HC1 in the gas- tric secretion compels the individual to lead the life of a patient. But over and beyond this, Flint (, loc.cit .), Fenwick (“The Lancet,” 1877), Quinke (“ Samml. klin. Vortrage,” No. ioo, 1876), Nothnagel (“ Deutsch. Arch. f. klin. Med.,” Bd. xxiv, 1879), Osier (“ Amer. Jour. Med. Sciences,” April, 1897), Kinnikut (“Amer. Jour. Med. Sciences,” October, 1887), also Rosenheim and G. Meyer (both in article on “Achylia,” by Martius and Lubarsch), have described cases of pernicious anemia in which atrophy of the gastric mucosa was, at the autopsy, found to be the only organic disease existing. It is conceivable that the intestine can not persistently digest an amount of proteid sufficient to maintain the nitrogen equilibrium during work ; that it depends upon a certain part of this prote- olysis to be performed by the stomach ; that the acid gastric chyme is necessary for the stimulation of the duodenal secretions. It is probable that digestion in the duodenum is not perfect without the acid protoids, which, as we know, cause increased diastatic action of the pancreatic juice (B. K. Rachford, “Am. Journ. Physiol.,” vol. 11, p. 494, July, 1899). So I take the ground that the supplementing of HC 1 is rational, even if we can not supply the deficit, because the amount necessary thereto could not expediently be administered. If we can not always add sufficient HC 1 to make the chyme distinctly acid, we can at least add enough to disinfect it and free it from a part, the surplus, of its germs, and perhaps produce some of the preliminary stages to peptone; for the acid albumins (syntonin) and propeptones are absorbable, and those not absorbed, we believe, are of some further utility in duodenal digestion. This conclusion is based upon quantitative analyses of human duodenal contents, from cases of achylia gastrica and from normal individuals. In some cases, however, we are enabled to add enough to give the reaction of free HC1 to the chyme. According to Honigmann and von Noorden (“ Zeitschr. f. klin. Medizin,” Bd.xm),one part by weight of pure HC 1 is able to satu- rate 18 parts by weight of egg-albumen ; 100 drops of dilute hydrochloric acid, containing 12.5 per cent, of the absolute HC1, will suffice to digest 15 gm., or 225 gr. — little less than 4 drams of pure egg-albumen. Riegel cites this statement (Joe. cit., p. 258), evidently to show how inefficacious 100 drops of a 12.5 per cent. DIGESTIVE POWER OF THERAPEUTIC DOSES OF HCl. 33 1 solution of HCl are as a digestive. (The dilute hydrochloric acid of the U. S. Pharmacopeia is a ten per cent, solution.) The conclusions of Honigmann and von Noorden, however, are, in our opinion, not calculated to inspire therapeutic skepticism. An amount of proteids equal to 4 drams of dried egg-albumen is a considerable quantity to be relieved of, and it can not fail to ease gastric digestion to give the acid, even if it can do no more work than this. But then it is practicable to give more than 100 drops of dilute HCl if necessary. Furthermore, the albumen molecule need not be saturated in order to become absorbable, as we shall see. Not near so much HCl is required for the formation of acid albumen as for that of hemialbumose or peptone. Riegel himself succeeded in causing a resumption of secretion of HCl in a patient who had not shown any for months, after he had taken 1.5 gm. of hydrochloric acid daily for fourteen days. He believes, however, that diet and lavage may have had much to do with the recovery. Reichmann and Mintz (“ Wiener klin. Wochenschr.,” 1892) report several cases in which free HCl could be again demonstrated after it had been missing for a prolonged time ; the resumption of HCl secretion was attributed by them to a prolonged dosage with the same acid. As we shall see in the chapter on Achylia, this dis- ease may depend on a number of very different factors. Sometimes there is no evidence of pathological change in the mucosa, and naturally these may readily recover (neuroses), even without HCl treatment. Professor Biedert claims to have used 120 drops of dilute HCl daily for a number of years, with much benefit to his achylia (Biedert and Langermann, “ Diatetik u. Kochbuch f. Magenkranke,” 1895). Hanni introduced into the stomach 400 c.c. of a 2.5 : 1000 solution of HCl, containing also 2 gm. of pepsin, together with an Ewald test-breakfast. As early as fifteen minutes afterward, when some of the test-meal was withdrawn, the free HCl had completely disappeared and the digestive power of the sample was equal to zero (Hanni, “ Zeitschr. f. klin. Med.,” Bd. xix, Supple- ment^. 307); and Boas cites this statement to show that the diges- tive value of HCl therapy is doubtful. Now, a patient who gets rid of 400 c.c. of liquid in fifteen minutes has hypermotility ; so much could not possibly be absorbed in that short period (the stomach does not absorb dilute HCl solutions). Nor could all of 1 gm. of absolute HCl which 400 c.c. of a 2.5 : 1000 solu- 332 IMPORTANT MEDICINAL AGENTS IN GASTRIC THERAPY. tion contain enter into combination with the proteid of a single roll; for ioo gm. of wheat roll contain only 7 gm. of nitrogenous or HCl-binding materials. We know, however, that 1 gm. of absolute HC 1 can digest 18 gm. of dried egg-albumen. There- fore the 400 c.c. had probably all been rapidly expelled into the duodenum before they could even be thoroughly triturated with the test-breakfast. This does not occur normally, and we are not justified in drawing conclusions from such hyperkinetic cases regarding the value of HC1 therapy. As the amount of absolute HC 1 introduced in Hanni’s experi- ments equaled 1 gm., and as so much could not enter into com- bination with the proteid of one roll, or 100 gm. of wheat bread, it stands to reason that if the motility had not been so exaggerated, some of the HC 1 would have been regained. Whenever Hanni {loc.cit., p. 306) succeeded in regaining some of the solution of HC 1 after it had remained in the stomach forty-five to sixty minutes, or even thirty minutes (see cases No. 3, Schmid, and No. 4, Hanni, p. 307, loc. cit .), the tests for HC 1 were positive and fibrin was well digested by the filtrate. The experiments of von Mehring, Moritz, and myself apparently agree in permitting the deduction that fifteen minutes is an abnormally rapid time for the expulsion of 400 c.c. of liquid (even if it were only water) into the duodenum, and whenever there is a fuller meal given than a simple test-breakfast, this rapid expulsion does not occur, because solid and semisolid matter can not be moved out so readily. Again, we must make allowance for a certain unavoidable nervous tension, and for the influence of suggestion, which takes hold of patients under experi- mentation, and which, from experience, we know has a decided influence on the rate of peristalsis. A careful series of analyses, constituting a rational basis for HC 1 therapy, is that of Charles E. Simon (“ The Modern Aspect of Indicanuria,” “ Amer. Jour. Med. Sciences,” Aug., 1895, p. 170). We submit a number of his conclusions : “(1) The gastric juice possesses antiseptic and germicidal properties. “ (2) These properties are referable to the presence of free hydrochloric acid. “(3) A subnormal amount of free hydrochloric acid will call forth an increased degree of intestinal putrefaction. “(4) The conjugate sulphates form an index of the degree of intestinal putrefaction. INDICATIONS AND CONTRAINDICATIONS TO HCl THERAPY. 333 “ (5) The increased intestinal putrefaction in cases of subacidity and anacidity of the gastric juice is largely referable to an increased formation of indol. “ (6) The elimination of indican in the urine may be regarded as an index to the amount of free hydrochloric acid present. “(7) A normal acidity of the gastric juice is never associated with increased indicanuria. “ (8) Cases of ulcer of the stomach apparently form an exception to this rule, an increased indicanuria being usually associated with hyperchlorhydria. “(9) In other cases of hyperchlorhydria a subnormal or normal amount of indican is eliminated.” We therefore recommend hydrochloric acid, believing in its efficacy in supplementing the digestive work of the stomach. Whenever it is indicated, we usually give 20 drops of the diluted HCl (U. S. Pharm.) in 2 ounces of water every half hour, beginning fifteen minutes before the meal; then 20 drops are taken during the eating, and 20 drops one-half hour after the meal. The medicine should always be taken through a glass tube, and the mouth rinsed with a weak solution of sodium carbonate afterward. As a remedy for improving the appetite, HCl is conceded, even by those skeptical of its digestive power, to be of value. For this purpose it is best given in small doses diluted with water (10 to 20 drops in 3 ounces H 2 0 ), on an empty stomach, before meals. With regard to its disinfectant and antifermentative effect I entertain serious doubts, since it can not be given in sufficient quantity to be of much benefit in that direction when given with meals. Whenever there are decided fermentations in the stomach, lavage is the most efficient means of combating it, and for this purpose HCl in the form of a 6 : 1000 solution may be used. Hydrochloric acid is contraindicated when the normal gastric secretion is augmented. We have observed cases in which there was no free HCl to be detected by Congo paper or phloroglucin- vanillin, but HCl given per os produced gastric distress and pain ; so that there can be no doubt that cases of hyperesthesia toward HCl exist analogous to those described by Talma (“ Zeitschr. f. klin. Med.,” Bd. vm), which do not depend upon hyperchylia. One female patient could detect whenever 8 drops of the diluted acid were given surreptitiously in the meals or medicine, by the gastralgia caused thereby. This was a highly neuropathic case. 334 IMPORTANT MEDICINAL AGENTS IN GASTRIC THERAPY. The amount of HCl consumed in the digestion of albumin has been very carefully studied by Fleischer. It takes 0.05 gm. of HCl to transform 1 gm. of egg-albumen into acid albumen. As human beings frequently take in 150 gm. of egg-albumen in twenty-four hours, it would require 7.5 gm. of pure HCl (or 30 gm. of the 25 per cent, solution of the laboratories) to transform this amount into acid albumin. As the gastric juice contains HCl to the amount of 2 per mille, 3 y 2 liters of gastric juice would be required to digest that amount of egg-albumen. Many children consume about one liter of milk daily; this would require 4.5 gm. of pure HCl or 18 gm. of a 25 per cent, solution of HCl (100 gm. of cows’ milk com- bined with 0.45 gm. of HCl). These amounts of HCl would bring the ingested albumen only to the stage of acid albumin or syntonin ; but as hemialbuminose and peptone would require twice the amount of HCl, the quantity combined with must eventually be increased beyond the figures stated. A portion of the albuminous foods passes over into the intestine, however, and there is digested long before it reaches the stage of hemialbuminose; but when the transit of the food into the duodenum is obstructed, it is evident that enormous quantities of HCl must be secreted to digest all the albumin that is taken in. For a purely physiological reason, it is not possible that the glandular layer can secrete the requisite amount. The absence of free HCl in these cases may be due to an invasion of the mucosa by the disease causing the pyloric obstruction. It is not impossible, however, that, even without this invasion, the mucosa has become exhausted, its secretory function being paralyzed. The Alkalies. — Probably the earliest experiments upon the effect of alkalies on the gastric secretion are those by Claude Bernard, who found that in small doses they increased the secre- tion of, and in large doses they neutralized, the gastric juice in animals. Leube (in von Ziemssen’s “ Handbuch,” Bd. vii) stated, as a result of experiments on dogs with gastric fistulae, that the car- bonate of soda of the Carlsbad springs not only neutralized an excess of acid, but could cause a lasting increase in the HCl formation of a diseased mucosa. Du Mesnil (“ Deutsch. med. Wochenschr.,” 1892), and Linossier and Lemoine (Academie de Medecin de Paris, session of March, 1893) agree in stating that when sodium bicarbonate is given together with a test-breakfast, or shortly before it,, it acts as an ACTION OF ALKALIES ON SECRETION. 335 excitant to the mucosa and increases the percentage of HC1 formed. In a case of hyperacidity, however, Du Mesnil found that the amount of HC 1 was at once reduced. Indeed, the results of various experimenters differ according to the normal or abnormal state of the stomach with which they worked. It makes much difference, also, whether an alkali is given on an empty stomach, with very little or no secretion, when it may possibly act as an irritant to the mucosa and set up a secretory reaction, or whether it is given at the height of digestion and meets with free HC 1 ; it the latter case it must of necessity combine with the acid, and can cause no further secre- tion. It is unfortunate for the evolution of truth in this question — whether or not small doses of alkali can stimulate secretion — that quite a number of experimenters (Ewald and Sandberg, Leube, Spitzer, etc.) worked with Carlsbad salts or water instead of with a chemically pure simple salt. The people of other countries do not share that intense interest in the Carlsbad and other springs with the physicians of Europe ; or at least those of Germany and Austria. There are not a few prominent representatives among the Ger- man clinicians who have expressed grave doubts whether the cures and improvements reported are really due to the waters of Carls- bad, but that the credit must be given to the avoidance of bad home influences, the careful diet, the regular life, pure air, good sleep, and abstinence from alcohol (see pp. 3 13-3 15). Personally, we consider it our duty to emphasize that the waters of the Congress and Hathorn Springs, of Saratoga, N. Y., and of the Bedford Springs, in Pennsylvania, have produced similar marked improve- ment, and, when this was not possible, great alleviation of gastric symptoms there treated. But even here it is impossible to ignore the good which the strict observance of the factors of hygiene and diet above mentioned may have worked. The natural Carlsbad Sprudel salt has the following composi- tion, according to Prof. E. Ludwig : Sodium sulphate, 41.62 per cent. Potassium sulphate, 3.31 “ Sodium bicarbonate, 36. 11 “ Lithium carbonate, 0.2 “ Sodium chlorid, 18.19 “ Sodium borate, 0.03 “ Water, 0.44 “ 336 IMPORTANT MEDICINAL AGENTS IN GASTRIC THERAPY. The artificial Carlsbad salt, which, according to Boas, can fully replace the more expensive natural salt, contains the following salts, according to the German Pharmacopeia : Sodium sulphate (dried), 44 parts. Potassium sulphate, 2 “ Sodium chlorid, 18 “ Sodium bicarbonate, 36 “ In hyperchylia and hypersecretion (in gastric ulcer) it is given in doses of one to two dessertspoonfuls in of a liter of water, to reduce the excess of HC 1 and promote evacuation. In gastritis it is also recommended, and this has seemingly given the Carlsbad enthusiasts much difficulty, namely, to explain how the identical solution may produce reduction of the HC 1 , and in another case promote HC 1 formation. We have studied eight cases who went to Carlsbad suffering from subacidity and from achylia; we have not, in a single instance, observed a return of secretion where it was lost or an increase where it was deficiently formed. Reichmann is one of the few who objected to applying the deduc- tions found with Carlsbad water or salts, on account of their com- plexity to the effects of pure, simple alkaline salts (“ Therapeut. Monatshefte,” 1895). We have never shared the opinions of thsoe who believe that small doses of alkali given on an empty stomach can produce a reactive secretion of HC 1 which may exceed the amount necessary to combine with the alkali given. We can understand that strong solutions of sodium and potassium sul- phate, such as the Carlsbad water, may actually play the role of an irritant, to which the mucosa responds in the form of an increased secretion, just as the nasal mucosa would do if a crystal of salt were placed in the nasal passage. Indeed, N. Reichmann declares, after a series of careful analyses with Na 2 C 0 3 , that the bicarbonate of sodium does not act upon the secretory inechairism of the stomach , but only upon the juice already secreted , by neutralizing it and render- ing the gastric contents alkaline (Boas, “ Archiv f. Verdauungs- krankh.,” vol. 1, p. 44). The actual therapeutic application of alkalies, therefore, is limited to those dyspepsias associated with increased HC 1 formation, in simple neurasthenic hyperchylia, in hypersecretion, and in gastric ulcer. They are indispensable for lavage when it becomes neces- sary to neutralize acids and dissolve adherent mucus. The time ADMINISTRATION OF ALKALIES. 337 to give alkalies in hyperacidity is from one-half to one hour after meals, when the HC 1 secretion is quantitatively at its height. The sensations of the patient are a very good guide, and the time can be learned by experience; the alkali should then be given a little previous to the time when the gastralgia, eructation, pyrosis, and distention set in. In hypersecretion there is a large amount of HC 1 present almost continuously in the empty stomach, in addition to hyperacidity after meals, so here we should give alkalies before meals in order to insure a certain time for action to the ptyalin ; for this constant secretion a glass of Saratoga Vichy, or simply sodium bicarbonate, 5j, in ]/ 2 of a pint of plain cold water, before meals, is sufficient to permit amylolysis. In ulcer and chronic gastritis acida, alkalies find application also (refer to treatment of these diseases). Determination of the Amounts of Alkalies Required . — Two groups of these bodies are in common use: (i) The alkaline earths ; (2) the alkaline carbonates. Of the first group, magnesia usta or calcined magnesia, and the more expensive magnesium ammonium phosphate are the favorites ; and of the second, the sodium car- bonate and bicarbonate. Those alkalies which are capable of com- bining with the largest amount of HC 1 are preferable. It is expe- dient to avoid excess of sodium bicarbonate, because the liberation of C 0 2 in the neutralization may cause annoying distention of muscular walls already infirm. Magnesia usta has the greatest binding power for HC 1 , and the reaction is expressed in the following equation : MgO + 2 HCI = MgCl 2 + 2 H 2 0 . Here 0.55 part of MgO correspond to one part of HC 1 . The reaction with ammonio-magnesium phosphate is the fol- lowing : Mg(NH 4 )P0 4 4- 3 HCI =r MgCl 2 + NH 4 C1 4- H 3 P0 4 . Calculation here gives the result that 1.25 parts by weight of Mg(NH 4 )P 0 4 correspond to one part by weight of HC 1 . The reaction with sodium bicarbonate is as follows : NaHC0 3 4 - HC1 = NaCl + H 2 0 4- C0 2 . Calculation of the molecular weights shows that 2.3 parts of NaHC 0 3 correspond to one of HC 1 . According to Boas, the dose of sodium bicarbonate necessary to counteract a superacidity exceeding 2.5 : 1000 is eight to ten gm., or four to six gm. of ammonio-magnesium phosphate, or two to 338 IMPORTANT MEDICINAL AGENTS IN GASTRIC THERAPY. three gm. of magnesia usta. With an acidity of 3 : 1000 HC 1 , the NaHC 0 3 can be increased to twelve gm., the ammonio-mag- nesium phosphate to 7.5 gm., and the magnesia usta to five gm. These calculations are made upon an amount of stomach contents equal to 400 c.c. ; but as a part of the alkali is expelled into the duodenum, another part absorbed, and as the momentary quantity of HC 1 present can only be reckoned upon, the figures may be too low. With constipation and collection of gas in the intestines the preference is to be given to the magnesia salts. Germain See (“ Semaine Medicale,” 1890, No. 12) recommends the following: R. Sod. bicarb., Creta prsep. , Magn. carbon., . . aa 0.2 gm. M. Take at once. Boas’ formula for continued excessive secretion is the following : Metric System. R. Magnesise ustse, 15.0 gr. 231.5 Bismuth, carbon., Natrii carbon., aa 5-0 gr. 77 .2 Ext. belladonnse, Ext. strychn., aa o. 1-0.2 gr. 1.7. M. Sig. — O ne teaspoonful three times daily, half an hour after meals. The amount of HC 1 secreted should be watched and the alkali discontinued if it becomes normal. The Bitter Tonics and So-called Stomachic Remedies. — Experience has lent belief that the bitter tonics are agents which stimulate the appetite and the secretory and motor functions of the stomach. They are represented by preparations of condurango, quassia, Colombo, gentian, angostura, absinthe, nux vomica and strychnin, creasote, guaiacol, orexin, lupulin, cetrarin, erythrocen- taurin, rheum, resorcin, quinia, cinchona. Under certain conditions, HC 1 , sodium chlorid, and alcohol act as stomachics. Some writers class sodium bicarbonate among these remedies, upon the supposition that small doses of this alkali may stimulate secretion of gastric juice; this therapy is, in our opinion, falla- cious. As a general rule, these medicines are useful to improve the appetite, and as anorexia is mostly found in reduced or lost gastric secretion, the effect upon secretion is apparently the only one that can be attributed to them. What the bitter tonics really effect and how they act is an unsolved problem. There seems to be an absence of scientific exactness in many of the experiments, ACTION OF BITTER TONICS. 339 and a general diffusiveness regarding the special point of inquiry to be solved. Thus, Penzoldt pretends that genuine stomachics must be able to improve all of the gastric functions (Penzoldt, on “ Salzsaures Orexin,” “Therap. Monatsh.,” 1890, No. 2). Loss of appetite may be present when the functional work is reduced, and then bitter tonics would be indicated; but it may just as well be present with normal or morbidly increased functions when stomachics would do harm. For instance, we have had many cases of anorexia with hyperacidity where the appetite returned after the use of bromid of strontium. In dilatations with fermenta- tion the best stomachic is lavage. As every disturbed function or disease requires elucidation, so the anorexia based thereon demands its own adapted treatment. Bitter tonics and allied medications are, in general, stimulants to the mucosa, and although they have a large application, it is not rational to use them empirically. A sedative or an antiseptic may, under certain conditions, be a better medicine than the bitter tonic for anorexia. The most rational course to pursue is to ascertain the exact state of the gastric func- tions, and after the establishment of the diagnosis attempt to remove the cause of the anorexia, whether it is depressed motility, accumulation of mucus, fermentation, or impaired secretion. For a fuller account of the physiological effects of these remedies the reader is referred to recent works on pharmacology and thera- peutics. The most useful medicines of this class, in my experience, have been strychnin and condurango, which, according to the experi- ments of L. Wolff, have no appreciable effect on the rate of secretion (“ Zeitschr. f. klin. Med.,” Bd. xvi, S. 222). Reichmann’s very carefully conducted investigations (“ Zeitschr. f. klin. Med.,” Bd. xiv, Heft. 1 und 2) brought out the fact that some bitter tonics failed to cause any secretion of gastric juice when distilled water did; and whenever* water failed to produce secretion, the bitter remedies failed also. On normal digestive processes these agents have no effect ; but when a juice was secreted that was acid, though not containing HC 1 , and if a gastric juice very weak in pepsin was secreted, then the bitter tonics, especially absinthe, were found to produce a stronger degree of acid and distinct reaction for HC1. Whenever there was atrophy of the glandular apparatus, all of these remedies failed to cause a secretion of gastric juice containing HC 1 . In brief, his conclusions are that the effect is very variable, sometimes less than that of water; but sometimes there is an in- 340 IMPORTANT MEDICINAL AGENTS IN GASTRIC THERAPY. crease of secretion after the bitter tonic has become absorbed and disappeared. They act best when given before meals, and when there is a gastric secretion still present, but J much reduced (hypo- chylia). In hypersecretion Reichmann found that the acidity was still further increased by bitter tonics. We advise that the bitter tonics should be given only in hypochylia or subacidity, and then one-half hour before meals. The author’s favorite formula for anorexia from hypochylia is the following : Metric System. B- Strychnin, sulphas, 0.020 Acid, hydrochloric, dil. , .... . 14.787 Ext. condurango fl. , 45.361 Elixir gentian. , q. s. ad 177.442 gr. 'A fgss f ^ iss f^vj. M. Sig. — O ne-half of a fluidounce in two ounces of water, one-half hour before meals, through a glass tube. Or— Metric System. B . Tinct. nucis vomic., 10. o fgiiss Essentiae calisayae (P. D. & Co.), . 60.0 f^ij Elixir gentian., q. s. 180.0 f^vj. Sig. — One-half of a fluidounce thrice daily, one-half hour before meals. M. When there are evidences of anemia with the hypochylia, the following acts satisfactorily : Metric System. B- Quininse sulphatis, I.I 93 gr. xviij Strychnin, sulphatis, gr- K Ferri sulphatis, . . o -775 gr. xij Acid, arseniosi., . O.OI 2-(- gr. i. M. Sig.- — Fiantpil. No. xij. One pill three times daily (must be prepared fresh and not coated). Boas uses the following powder for anorexia : Metric System. B- Ext. strychn., 0.03-0.05 Bismuth, carbon., 0.50 M. f. pulv. Dent. tal. dos. xx. SiG. — One powder three times daily. g r - | gr. viij. Menche has warmly recommended resorcin sublimate, and it undeniably improves the appetite in cases of incipient gastric fermentation. It has also a slight sedative action. The following is Menche’s formula: BITTER AND OTHER GASTRIC TONICS. 341 Metric System. R . Resorcin, resublim. 2.0 gr. 30.5 Acid, mur., 1.0 gr. 15.4 (Or, if it be indicated in place of the HC 1 , one may order Natr. bicarb., 8.0.) Aquae destil 180.0 fg v j Syr. simpl., 20.0 3 ”j- M. D. et ad vitr. nigr. SlG. — Fifteen c.c. (,^ss) every two hours. The following formulae are recommended by Ewald for anorexia with fermentation : Metric System. R. Tinct. nucis vom., . 25.0 f 3 v i Resorcin, resublim., . 5.0 gr. lxxxj Tinct. amar. , Take ten to fifteen drops every two hours. . 10.0 f 3 iij- R. Ext. condurang fl., f 3 ivss Resorcin, resublim. , SlG. — Thirty drops four times daily. . 4.0 M. M. Creosote is a remedy of doubtful efficacy in my experience, as it rarely benefits digestion except in tuberculous patients. Wegele says ( loc . cit. f p. 53) that it will help if it is tolerated and causes no severe dyspeptic difficulties, but the latter is just what it will do in more than one-half of the cases. I have my doubts whether it can promote peristalsis, as is asserted by Klemperer (“ Centralbl. f. klin. Med.,” 1891, No. 21), until enough is given to act as an irritant. Even when it is tolerated by the stomach, the repeated penetrating eructations are very annoying to patients. Sommer- brodt recommended it to be taken in capsules. Bouchard advises the following formula : Metric System. R. Creosot. puriss., 13.5 Tinct. gent., 20.0 Vin. Xerens, 800.0 Spir. rectif. 200.0 M. SlG. — One-half of an ounce four times daily. Orexin (phenyldihydrochinazolin) has been strongly indorsed as a “ genuine ” stomachic by Penzoldt. In 273 cases he observed 144 successful restorations of appetite and secretion. Its special indications are gastric atony and beginning gastritis, and its action is attributed to its power of increasing the secretion of HC 1 (Pen- zoldt, “ Weitere Mittheilungen liber Orexin basicum,” etc., “ Therap. 342 IMPORTANT MEDICINAL AGENTS IN GASTRIC THERAPY. Monatshefte,” May, 1893). The following formula is advised by Penzoldt for this useful drug: R. Orexin basic., gss, or 2 gm. SiG. — Divide into six powders; inclose in small wafers. One to be taken in a cup of bouillon half an hour before meals, twice daily. Digestive Ferments. — Artificial means of aiding digestion are certainly much abused, and if employed for long periods, they fre- quently become, to a certain extent, injurious. Every organ is strengthened by activity and weakened by lack of exercise. The stomach will grow weaker and weaker the more artificial gastric juice is poured into it, and the finer and more subtle the nourish- ments are that are allotted to it. This agrees in the main with what we stated under Dietetics, namely, that the diet should not be leveled down to the digestive capabilities of the stomach, but that digestion should be leveled up until it can deal efficiently with the amount of food required for the nitrogen equilibrium. In truth, the indiscriminate dosing with digestive ferments does more harm than good. The stomach is an organ which very rapidly adapts itself to cease performing the work that is done for it arti- ficially. Then, again, there is such a thing as educating an appa- rently weak stomach up to digesting food which at first seems in- digestible, and is taken with “ fear and trembling.” So we will find that gastric training (gymnastics of digestion) by graded diet may favor the development of what fragments of glandular ele- ments may yet be slumbering in a diseased mucosa, but the ir- rational use of ferments may, by doing all the work itself, permit the gland-cells to go on to atrophy. The artificial ferments have been recommended when there is a deficiency or absence of the natural secretion. They may be con- sidered in two classes : (1) Those that have been isolated from the mammalian organism — viz., ptyalin, pepsin, pancreatin ; and (2) those derived from the vegetable kingdom — viz., the various dias- tases, papain, bromilin. Some of the ferments of the human body have not yet been isolated ; these are the milk-curdling ferments of the gastric and pancreatic juices and the emulsifying and fat-split- ting ferments. There are ferments in the succus entericus (invertin, etc., perhaps a curdling ferment) which we understand very little. Ptyalin . — This ferment of the saliva is indicated in hyperacidity and hypersecretion, when the normal ptyalin may actually be destroyed in the stomach. Boas has shown that with diminution of the acidity SO-CALLED AMYLACEOUS DYSPEPSIA. 343 this ferment may, to a degree at . least, resume its inversion of starches into dextrose. With very intense hyperacidity (0.04 : 1000) the ferment appears to be so injured that it can not be restored to function, and a new supply may be necessary. Ptyalin is given in doses of five to fifteen grs., with 3j of sodium bicarbonate, immediately after meals. There can be no doubt of the greater amount of dextrose formed with the aid of ptyalin, and these patients are thereby enabled to eat more of carbohydrates. Diastase . — Malt diastase, as manufactured in the form of liquid extract, or in dry form, as in Horlick’s diastoid, is serviceable for the same purpose. Professor Leo, of Bonn (“ Therap. Monatshefte,” Dec., 1896), reported to the Congress of German Naturalists and Physicians on taka diastase, an American product, which appears to have strong starch-inverting power, and to be able to act in an amount of acid equal to 0.1 per cent. HC 1 . We have assured ourselves that amylolysis is effectually carried out by this taka-diastase, but the addition of an alkali is necessary, as with ptyalin, to render the effect prompt. Its tastelessness and moderate price are in its favor. Ewald has found, in a great many observations, that absence or deficiency of ptyalin is exceedingly rare; so that ptyalin is rarely required because it is secreted in sufficient quantity, but in some way it may be destroyed. The hygiene of the mouth should receive careful attention ; a septic or acid mouth, with coated tongue and bad teeth, will offset any amount of ptyalin. To treat “ amylaceous dyspepsia ” — which is the objectionable name given to symptoms of hyperacidity and hypersecretion — by cutting off the carbohydrates is irrational, because they can not be dis- pensed with, not on account of the starch only, but on account of the proteid which amylaceous foods contain. It will be found, from the army rations of men under service of various nations, that the carbohydrate portion of the foods is increased with harder work much more than the proteid and fat portion (see tables in Gilman Thompson’s “ Dietetics ” and Munk and Uffelmann’s “ Ernahrung des Menschen ”). Therefore these foods should not be taken away because they may not be perfectly digested ; but the cause of the indigestion should be, if possible, removed. If possible, a large amount of natural saliva should be swallowed after meals; many times have we observed that, with the simple supply of additional saliva caused by chewing a piece of rubber, starch indigestion could not be demonstrated in the test-meal, although it had 344 IMPORTANT MEDICINAL AGENTS IN GASTRIC THERAPY. existed before. To Fothergill is attributed the saying that ferments are crutches; no doubt many an invalid would prefer walking on crutches than not at all. There are many crutch-walkers, however, who, by modern surgery, have been enabled to throw them away and walk by themselves unaided. Just so with the ferments ; they may be used with success temporarily, but the best thing to do is to discover how the patient may digest without them. Pepsin . — There is no lack of pepsin preparations in the market, and their digestive powers, as claimed, seemingly have no limit. Certain very popular compositions of pepsin should be emphatic- ally condemned. For instance, all wines of pepsin are inefficient because very little of this ferment is taken up by alcohol. Recently a preparation was brought to our laboratory containing hydrastis, rhubarb, pepsin, and pancreatin in one solution, showing a total disregard for the physiological fact that pepsin acts only in an acid and pancreatin in an alkaline medium. There is rarely any indi- cation for the use of pepsin, for, whenever a test-meal shows free HC1, pepsin must of necessity be present in sufficient amounts; and even when HC1 is absent, pepsin or pepsinogen are, as a rule, still present. Assuming a case in which the last vestige of even pepsinogen secretion has been lost, the introduction of the ferment might be of utility, but the enormous quantities of HC1 necessary to bring about proper action of this pepsin could not be tolerated by any diseased stomach (see chapter on the Therapy of HC1). And, again, in cases where pepsinogen is still formed, the addition of HC1 simply will suffice to convert it into the complete ferment. Pepsin is prescribed much too often; personally, I have ceased using it. Pancreatin . — Although there are many preparations of this fer- ment, and some of them very active, the substance spoils and loses its digestive power with age. As it is an easy matter to test its amylolytic and tryptic power in artificial digestion experiments, it is wise to do so in all cases where much dependence is placed in its action. The nature and value of the substance were scientifically explained by Sir William Roberts (“ Digestion and Diet,” p. 66). It can be obtained in a liquid form as well as in the form of a dry powder, from extraction of the pancreatic gland of animals. This ferment is completely destroyed in the gastric juice. This is why thinking practitioners should not use both pepsin and pancreatin together in the same solution, because the medium in which one must act is opposed to that of the other. In the majority of cases PANCREATIN — INDICATIONS FOR ITS USE. 345 where pancreatin is given empirically, HC 1 is still secreted in the stomach and the ferment is destroyed. Gilman Thompson ( loc . cit ., p. 333) suggests that the pancreatin be inclosed in keratin cap- sules. Keratin is unaffected by gastric juice, but readily dissolves, it is claimed, in alkaline media. Hence the pancreatin may pass through gastric digestion, and at its completion pass into the in- testine, where the coating is supposedly dissolved and the ferment acts upon the chyle. The suggestion of Thompson was previously carried out by Unna. But this idea is not supported by experi- ment nor by exact indications of the conditions for the employment of pancreatin. Keratin will not dissolve in the duodenum except very slowly; pills coated therewith are found in the stools during normal digestion. There is no necessity for attempting to supply the ferment directly to the duodenum, since in the greater majority of cases, perhaps all, except when malignant neoplasm, cirrhosis, or abscess has destroyed the gland, there is plenty of pancreatic juice in that part of the bowel. In exceedingly rare cases pancreatic calculi and diseased states of adjacent parts may stenose the duct. In all these attempts it is overlooked that the reaction of the nor- mal duodenum is acid and will not permit the solution of keratin. There is but one distinct indication for the use of pancreatin, and that is permanent deficiency or complete absence of HC1 and enzyme formation of the stomach. Experiment and experience have conclusively shown that when pancreatic digestion is started in the stomach in these cases, by giving the pancreatin with sodium bicarbonate, there is a more exhaustive utilization of the proteids and carbohydrates. We have frequently assured ourselves of this fact by analyzing the stools after weighed amounts of these food- substances had been ingested, at the same time making identical analyses with the same amounts of proteid and carbohydrate, but with pepsin hydrochloric acid as an artificial digestant ; under the latter more food-substances passed through undigested than when pancreatin was used. Pepsin and hydrochloric acid naturally suggest themselves in atrophic gastritis, but judging from our observations, pancreatin is preferable. I have noticed cases in which there was a remark- able hypersensitiveness to hydrochloric acid even in doses of six drops of the dilute form, so that its use had to be dispensed with. The dose of pancreatin is from four to eight grains, together with the same amount of sodium bicarbonate in form of compressed tablets ; of these, two to four are taken fifteen minutes after meals. 23 34^ IMPORTANT MEDICINAL AGENTS IN GASTRIC THERAPY. Papain, Papoid, Papayotin . — These ferment>containing substances are made from the milky juice of a tree belonging to the family of Papayaceae, native in Central and South America. Bouchut and Wurtz (“ Sur la ferment digestiv du Carica Papaya,” “ Compt. Rend.,” 1879, tome lxxxix) first prepared papain, and later Peckolt brought out papayotin. Papoid, an American preparation, according to Prof. R. H. Chittenden, is a vegetable ferment made up of vegetable globulin, albumoses, and peptone, with which are associated the ferments characteristic of the preparation. Papoid has the power of digesting to a greater or less extent all forms of proteid or albuminous matter, both coagulated and uncoagulated ; its digestive power is exercised in a neutral, acid, as well as alkaline medium. Papoid is found in the stools, showing that it is not destroyed in the alimentary canal ; the dose is from one to three grains after each meal. Finkler prefers papain to pepsin for aiding gastric digestion (“ Therap. Gazette,” 1887, August 15th), and G. Littmann has observed good results with it in acute and chronic gastritis, dilata- tions, carcinoma, and dyspepsia after chronic ulcer (Littmann, “ Munch, med. Wochenschr.,” 1893, No. 29). Papain seems to be a variable product and its digestive action not always the same (Rossbach and A. Eulenberg). It is an expensive preparation. Recently a highly concentrated extract of carica papaya has been brought into the market under the name of caroid , which, according to Chittenden, has even a greater digestive power than papoid, and digests proteids, albumins, and starches in any medium. We append Chittenden’s results with this energetic ferment, concerning the clinical application of which further obser- vations are necessary : With 0.05 per cent, hydrochloric acid : Caroid, Undigested residue. Proteid digested. 20.2 per cent. Papain, A, 0.8959 “ 10.9 “ Papain, B, 0-8735 “ 13. 1 “ With 0.5 per cent . sodium bicarbonate : Undigested, residue . Caroid, 0.4596 gm. Proteid digested. 54.3 per cent. Papain, A, 43-4 “ Papain, B, O.5927 “ 41.0 “ If we examine these results critically, it is plain that the digestive power of caroid on proteid matter is greater than that, of the other PROTEOLYTIC FERMENT OF THE PINEAPPLE. 347 two preparations. The difference in digestive strength is more apparent in these experiments with coagulated egg-albumen than with the other form of proteid matter, although quite marked with blood-fibrin. 2. Starch-digesting Poiver . — In starch-digesting power caroid is far superior to the other preparations, either papoid or papain. The following experiments will throw some light upon this point A starch paste was made from five gm. of dry arrow-root starch with 500 c.c. of water. Mixtures were then prepared as follows : 1. 0.5 gm. of caroid, -(- 90 c.c. water -f- 10 c.c. of starch paste. 2. 0.5 “ “ papoid, + “ <<_)_<< “ “ “ 3. 0.5 “ “ papain, A, -f “ “ + “ “ “ “ 4. 0.5 “ “ papain, B, -j- “ “ “ « “ “ These four mixtures were placed at 40° C., and tested from time to time with iodin solution. In five minutes No. 1 had reached the achromic point, while No. 2 did not give the achromic reaction until at the end of two hours. At the end of three hours Nos. 3 and 4 still gave a bluish-violet reaction with iodin. In another series of experiments exactly similar to the above, except that each mixture contained only 0.2 gm. of ferment, the caroid brought about a complete conversion of the starch into bodies non-colorable by iodin in eighteen minutes, while the others gave a blue reaction after two or three hours. The presence of alkalies retards the diastatic or amylolytic action, but the caroid shows throughout very much greater amylolytic power than the other preparations. The Ferments of the Pineapple. — This fruit contains very active proteolytic ferments, its juice being used in the production of the artificial predigested beef foods by a prominent American firm. The ferments are destroyed by boiling, and hence are no longer active in the preserved fruit. We have assured ourselves suffi- ciently of the proteolytic activity of raw, fresh pineapple-juice to recommend it in achylia or subacidity, and to forbid its use in hyperacidity and hypersecretion, as well as in gastritis acida. It is allowed mainly because of its pleasant taste and because it stimulates desire for other food. The fiber must be removed from the mouth after chewing, and only the juice swallowed. 348 SURGICAL TREATMENT OF ORGANIC GASTRIC DISEASES. CHAPTER VII. SURGICAL TREATMENT OF ORGANIC GASTRIC DISEASES. In the preantiseptic time the stomach was regarded as a “ Noli me tangere.” Even in the beginning of this century gastric wounds were considered as necessarily fatal. Larrey, the Surgeon- General of Napoleon, was one of the first to declare, “ Plaies de Pestomac ne sont pas mortelles dans tous les cas ” (cf. “ Clinique Chirurg.,” tome iv, p. 10), which was, as is well known, confirmed by the notable observations of our countryman, Beaumont, on Alexis St. Martin. Not only were surgeons timid about the almost unavoidable peritonitis, but there existed a universal belief that the solving and peptonizing action of the gastric juice prevented the wound from healing. The observation that undoubted gastric ulcers had healed, and that gastric fistulse produced by physiolo- gists in animals healed spontaneously, and that gastrotomy and gastrostomy performed in preantiseptic years had not shown the corrosive effect of the gastric juice, paved the way for experi- ments by Gussenbauer and von Winiwarter, proving that gastric wounds, when sutured, healed, as a rule, without interference from any digestive action of gastric juice. The first proposition to treat organic gastric diseases by operation was made by Merrem, who originated the resection of the pylorus (pylorectomy), and, after performing it on dogs, suggested it for human beings (Dan’l C. Theodor Merrem, “ Animadversiones quaedam chirurg. experim.,” etc., Giessse, 1810). This writer men- tions that a Philadelphia surgeon had already attempted pylorec- tomy on dogs and rabbits, but had been unsuccessful. Gussenbauer and von Winiwarter demonstrated later that this operation was technically feasible, and that removal of the pylorus was not dangerous to life (“ von Langenbeck’s Archiv,” Bd. xix, S. 347). They succeeded in showing that a certain per- centage of cases of pyloric carcinoma were indications for this opera- tion. Czerny and Kaiser confirmed these opinions, and the latter managed to heal and keep alive a dog from whom he had excised almost the entire stomach. As a surgical curiosity, Haberkant (“ Arch. f. klin. Chirurg.,” Bd. li, Heft 111, S. 484) mentions a total extirpation of the stomach by Dr. Conner, of Cincinnati, in a HISTORY OF GASTRIC SURGERY. 349 woman fifty years of age, who died before the esophagus could be united to the duodenum. This operation was done December 7, 1883, and was the first attempt at a total gastrectomy recorded. According to Rydygier, a surgeon named Torelli, in 1878, executed the first gastric resection in a man, removing a piece sixteen cm. long that had prolapsed from an abdominal stab wound (“ Centralbl. f. Chirurg.,” 1879, S. 398). In the same year Billroth brought about healing of a gastric fistula by exposing the stomach and suturing it (“ Wien. med. Wochenschr.,” 1881, S. 275). In January, 1881, Billroth executed the first successful resection of the pylorus for carcinoma. The first total resection for ulcer was performed by Rydygier, and the first partial resection for ulcer was made by Czerny in 1882. Both were successful. Pean executed a pyloric resection in 1879, before Billroth, and so did Rydygier in 1880, but both were unsuccessful. In the first publication of Billroth’s resection (“ Wien. med. Wochenschr.,” 1881, No. 6) Wolfler defined the limits of the usefulness of total resection as existing in the transition of the carcinomatous tumors to the pancreas and duodenum. Cases in which the carcinomatous infiltration extended beyond the hepa- duodenal ligament should be excluded from resection. From these indications the plan to a second operation arose — “gastro- enterostomy,” which is a type of entero-anastomosis (Maisoneuve), an artificial communication between the stomach and the jejunum, when the pyloric obstruction, for reasons given, can not be removed. In 1881 (September 28th) Wolfler performed this operation for the first time; but the very next case (performed by Billroth) was fatal, the patient dying with constant emesis of bile. The necropsy showed that the upward traction of the jejunal loop had caused what is termed a “ spur,” which returned the duodenal secretions (bile, etc.) into the stomach. The spur had divided the artificial gastro-intestinal lumen into two unequal parts, of which the larger belonged to the duodenal canal, the smaller to the jejunal loop leading away from the stomach. As a necessary result of this the bile and pancreatic juice ran into the stomach, while nothing could pass out into the diminutive discharging outlet. In one of Lauenstein’s cases (“ Verhandl. d. Deutsch. Gesell. f. Chirurg.,” Thirteenth Congress) the mesen- tery of the jejunal loop, which had been drawn up to meet the stomach, compressed the transverse colon. The adducent part of the loop was drawn across the colon like a tense ridge. Courvoisier, 350 SURGICAL TREATMENT OF ORGANIC GASTRIC DISEASES. in 1883, invented another method calculated to avoid these diffi- culties. Instead of inserting the jejunum to the ventral or an- terior wall of the stomach, he made a slit in the mesentery of the transverse colon and inserted the loop into the posterior gastric wall. In order to secure the continued onward flow of the bile and pancreatic juice through the intestine, Courvoisier attached the adducent part of the intact loop to the stomach for a distance, then split the abducent part, and finally sewed the wound edges of the gastro-intestinal opening. In 1885 von Hacker described a similar but much more improved meth'od, which consists in the following : The colon and great mesentery are raised upward ; the gaping edges of the slit in the mesocolon are attached to the posterior gastric wall ; finally, the jejunal loop is attached to the stomach within this slit (von Hacker, “ Verhandl. d. Deutsch. Gesell. f. Chirurg.,” 1885, Four- teenth Congress). A third method of gastro-enterostomy was suggested by Billroth and Brenner (“ Deutsche Zeitschr. f. Chirurg.,” Bd. xxv, p. 502). In this method openings are made both through the gastrocolic ligament and mesocolon, through which the jejunal loop was drawn up and sewed to the anterior gastric wall immediately above the greater curvature. Von Hacker has given these various operations very significant and explicit Latin designations (“ Chir. Beitr. a. d. Erzherzogin Sophienspital in Wien,” S. 42). These are his terms in English : 1. Gastro-enterostomy, anterior, antecolonic (Wolfler). 2. Gastro-enterostomy, posterior, retrocolonic (von Hacker). 3. Gastro-enterostomy, anterior, retrocolonic (Billroth-Brenner). A number of other modifications must be passed over, since we are interested only in the clinical, not so much in the purely sur- gical, aspect of the subject. Since the publication of the first edition of this work, in October, 1897, the subject of the “Surgery of the Stomach” has been re- viewed and represented in the “ Cartwright Lectures,” published in the “Phila. Med. Journal,” volume 1, pages 829, 927, 1053, and 1 104. This is a most comprehensive and conservative representation of gastric surgery, by one of the ablest operators and surgical philos- ophers of our country, Prof. W. W. Keen. A second very helpful publication bearing directly on this subject is the volume by Lindner and Kuttner — “ Die Chirurgie des Magens und ihre Indicationen einschliesslich Diagnostik.” GASTROLYSIS. 351 The lectures by Prof. Keen contain references to most of the important American and English works, and the volume of Lindner and Kuttner, the German aspect of the subject, though this is by no means neglected in the former. An excellent French representation of surgery of the stomach is by Professors F. Ferrier and Hartman, Paris, 1899. VARIOUS FORMS OF OPERATIONS PRACTISED UPON THE STOMACH. Gastrolysis is the name of an operation by which peritoneal adhesions binding the stomach to other abdominal organs and the abdominal wall are severed. The symptoms of gastric adhesions are variable and obscure, and the diagnosis is difficult. The most constant symptoms are: (1) A long history of digestive suffering; (2) persistent pain; (3) persistent vomiting; (4) displacement — in any direction, sometimes even upward. In one- third the cases of adhesions there is evidence of existing or pre- vious gastric ulcer. The author referred to a case of extensive adhesions in the first edition of this work (p. 695). A negro, 58 years old, had been suffering from the most intense gastralgia, and vomiting off and on for twelve years. Distention of the stomach with C 0 2 did not bring the stomach forward and out from the arch of the ribs. The electrodiaphany showed the stomach in a higher position than normal. The gastric contents showed marked hyperacidity. An operation was undertaken upon advice of the writer, the diagnosis not being established definitely, but stated as probably gastric ulcer with perforation. The stomach was found bound to the diaphragm by two broad adhesions, to the transverse colon at about its middle, to the liver and gall-bladder. There were also adhesions between the jejunal loops and a firm adhesion of the ascending colon to the abdominal wall. The adhesions to the liver and gall-bladder proved inseparable. No gastric ulcer was discovered at the operation, but an old cicatrix was found at the autopsy two months after operation. As a rule, the operation is successful. Of Lauenstein’s ten cases, nine recovered (“Arch. f. klin. Chir.,” 1892, xlv, 121). Other successful operations are reported by Robson, Naylor, Ferrier, Hoffmeister, Billroth, Mikulicz, and Hahn (“ Deutsch. med. Wochenschr.,” 1894, No. 43). The adhesions may reunite after intersection and cause renewed trouble. 352 SURGICAL TREATMENT OF ORGANIC GASTRIC DISEASES. Gastrotomy is the operation of opening the stomach with the object of removing a foreign body; then sewing up the wound in the stomach, replacing the viscus, and sewing up the external abdominal wound. This operation must be looked upon as very successful, for, of 18 cases reported by Henry Morris (Ashhurst, “ Encyclopedia of Surgery,” vol. v, p. 589), 14 recovered. This operation is also executed with a view to effecting dilatation of stricture of the esophagus from the stomach side; and, thirdly, the stomach is opened for exploratory purposes. Gastrostomy is designed to rescue a person from immediate starvation when there is a stenosis in the esophagus, either from cicatricial contraction resulting from esophageal ulcer, syphilitic, tuberculous, or malignant neoplasm, or corrosive toxic agents. Occasionally, this operation may be required by tumor outside the esophagus. Roswell Park (“ International Med. Jour.,” Jan. 9, 1894) and Stockton, also Whitehead, have done the operation for diverticulum of esophagus. The various methods of technic of this operation are described in the articles of W. W. Keen ( loc.cit ., p. 836). Andrews, Senn, and Stamm are American surgeons who have described new methods for this purpose. The same causes affecting the cardia — for instance, carcinoma of the cardia — may necessitate gastrostomy. Our experience is that the sooner gastrostomy is performed in carcinoma of the cardia, the longer is the life sustained. One should not wait until noth- ing but liquids will pass the stricture. It has been observed that the carcinoma will improve and show some tendency toward healing when food no longer passes over it and the dilatation above the stricture is kept clean by esophageal lavage. When- ever possible, the esophageal dilatation should be washed out daily, even after gastrostomy has been performed. In cases where the esophageal stricture had become impassable, it has occasionally been noticed that after gastrostomy the stenosis again became permeable, and food could be swallowed for a while. Witzel has devised an oblique entrance of the fistula into the stomach, making use of the anatomical relations of the abdominal walls for that purpose. The canal is laid partially in the gastric and partially in the abdominal walls, being somewhat tortuous, and mostly closed to food trying to come outward (Witzel, “ Z. Technik d. Magenfistelanlegung,” “ Centralblatt f. Chirurg.,” 1891, No. 32). Von Hacker’s technic, as original with him, has been practised in a number of cases for dilating esophageal strictures with sounds introduced from the GASTRORHHAPH Y. 353 gastric side, when dilatation of the strictures from the mouth had failed. The unfavorable results of gastrostomy — Zesas reported only 19.5 per cent, of so-called recoveries in 13 1 operations (“Arch, f. klin. Chirurg.,” Bd. xxxn) — are largely due to postponing the operation until the general health is too low to assist in recovery. Mikulicz has formulated his latest results in the following table (“ Arch. f. klin. Chirurgie,” Bd. Li, p. 9, 1895): GASTRECTOMY AND GASTROTOMY. Total. Recovered. Died. O 2 O Mortality Percentage 0.0 66.66 IOO.00 0.0 For simple ulcer, For ulcer and hemorrhage, 1 3 1 1 I I 0 For ulcer with perforation, Occlusion of pylorus with a gall-stone, . . . Total, 6 3 3 50.0 The results in gastrostomy for esophageal carcinoma are stated by Mikulicz (Joe. cit.) as follows : Of 28 patients that survived the operation longer than three weeks, 20 subsequently died of the fundamental disease. The shortest duration of life was three and one-half weeks, the longest twelve months, after the operation. The average duration of life after the operation was four and one-half to five months. GASTROSTOMY. Total. Recovered. Died. Mortality Percentage. Toxic, corrosive stricture of esophagus, . . 9 9 O 0.0 Neurosis (cardiospasm), 1 I O 0.0 Carcinoma of cardia or esophagus, .... 34 28 6 17.64 Total, 44 38 6 1363 Gastrorrhaphy, or gastroplication, is an operation for closure of wounds of the stomach. The term applies to any case where the stomach is sewed ; it is generally restricted to those cases in which a limited portion of the gastric wall is sutured with or with- out excision. The operation is available as a means of reducing excessive dilatations not complicated by malignant neoplasm and which have not improved under persistent and careful medical treatment. 354 SURGICAL TREATMENT OF ORGANIC GASTRIC DISEASES. Pylorectomy, or Resection of the Pylorus.* — In considering the value of this operation we must sharply distinguish between three types : 1. Typical, total, or circular pylorectomy. 2. Atypical pylorectomy, which consists of a combination of the former with a gastro-enterostomy. 3. Partial pylorectomy. Typical or Total Pylorectomy . — Indications in 259 operations were the following : Carcinoma, 215 times; ulcer or cicatrix, 34 times ; sarcoma, twice; angioma fibrosum, once; not stated, seven times. In judging of the benefit to be derived from these operations, we must distinguish sharply between (1) the immediate and (2) the remote results. Generally speaking, surgeons term a patient “ recovered ” when he succeeds in getting over the effects of the operation ; this is the immediate result. The remote results are determined by the duration of life after the operation. The imme- diate results of the 259 cases above enumerated are the following : Of 34 cases of benign stenosis, 23 recovered; of 215 cases of car- cinoma, 98 recovered ; both cases of sarcoma and the case of angioma fibrosum recovered. Haberkant (loc. cit .) found the mor- tality for ulcer to be 34.4 per cent., and for carcinoma, 56.7 per cent., in a total of 239 operations performed from 1879 to 1 ^ 94 - It is a very important question for the clinician whether the mortality is becoming less as time progresses, which signifies an improvement in the technic and knowledge of the subject. Haberkant arranged 205 cases, operated on from 1881 to 1894, in two series of seven years each (from 1881 to 1888, and from 1888 to 1895). In the first series the total mortality was 62.8 per cent. ; in the second series it was 45.1 per cent. For carcinoma a reduction of the rate of mor- tality from 65.4 per cent, to 42.8 per cent., and for benign pyloric stenosis a reduction from 42.8 per cent, to 27.7 per cent., is calcu- lated. In 1882, of 13 cases of resected carcinomata, all died ; in 1893, of 8 cases, all recovered. There may be some objection to the absolute correctness of these figures, but they undoubtedly admit the belief that our methods of diagnosis and operative technic * For the statistics and historical information on the subject of the principal operations we are indebted to the “Cartwright Lectures,” by Professor W. W. Keen, “ Phila. Med. Jour.,” vol. I, p. 931, and to an article by Dr. Haberkant in the “ Arch. f. klin. Chirurg.,” Bd. Li, p. 861, 1896; to a report by Prof. J. Mikulicz, “Arch. f. klin. Chirurg.,” Bd. Li, p. 9, 1895; the volume by Lindner and Kuttner (“ Magen Chirurgie,” and the work of Ferrier and Hartmann). PYLORECTOMY — RESECTION OF THE PYLORUS. 355 are improving. Some forms of gastric cancer are much more malignant and unfavorable to treatment than others. In 44 cases in which microscopical examinations were made, we found the following comparisons : Nature of the Gastric Cancer. Number of Operations. Recovered. Died. Scirrhus 16 IO 6 Adenocarcinoma (epithelial carcinoma), 10 5 5 Medullary carcinoma, 9 1 8 Colloid carcinoma, 9 7 2 44 23 21 According to this table, colloid carcinoma is the most favorable to operation, while the most unfavorable prognosis is to be formed of medullary sarcoma. The remote results are best shown in the duration of life after the operation, which is expressed in the accompanying table (see end of this chapter), from which it is evident that the average expectation of life after pylorectomy for carcinoma is not very long. For of twenty-six so-called recoveries, or immediate good results, seventeen, or nearly two-thirds, died within one year after the operation. Furthermore, of twenty- six (different) cases, twelve died in from one and one-half to thirteen months from return of the malignant trouble or metastases. One case of Billroth’s lived five and a quarter years. One case of Kocher (“ Centralbl. f. Chir.,” 1894, S. 221) lived five years and four months, and one case of Rat- timmow’s {ibid., S. 1014) lived eight years. Wolfler cites three cases who lived over four years, four over five years, one over six years, and two over eight years. The boundary of the pathological tissue can not be determined accurately. As is the custom in most malig- nant neoplasms of other organs, the resection is made by cutting through the apparently or visibly healthy tissue one cm. from the limit of the diseased portion. Czerny, however, found, by careful microscopical examination of resected pieces, that the edges of the section, made through apparently healthy tissue, contained cancer- ous alveoli ; he therefore advised that the cut be made not one, but three, cm. from the limit of the carcinomatous tissue. Virchow holds that as long as a neoplasm is solitary, the hope for a success- ful operation must not be given up. Pylorectomy is the only operation which can make a definite 356 SURGICAL TREATMENT OF ORGANIC GASTRIC DISEASES. cure or a recovery of some duration possible; and although the prospects of complete cure are very few, we must hold fast to the encouragement which statistics furnish — namely, that more cases recover with improvement in the technic and the possibility of early diagnosis. Haberkant ( loc . cit., p. 26) takes too gloomy a view of the future of gastric operations when he asserts that we must expect no advance in the curability of gastric carcinoma, because, in his opinion, patients decide for the operation too late, even after the diagnosis is certain ; and, secondly, because it will be impossible to diagnose gastric carcinoma at a time when a cure by extirpation would be possible. The early diagnosis of gastric carcinoma, he emphasizes, is in almost all cases impossible (?). The surgeon, as a rule, con- cludes to operate only when distinct stenotic symptoms are present, with emesis, dilatation, and palpable tumor. The only sign which Haberkant cites to be doubtful — that is, the absence of HC 1 in the gastric contents — is by no means the only one the clinician has to be guided by, as reference to the chapter on Diagnosis of Gastric Carcinoma will show. In justice to the surgeons, we desire to say that they are not given the cases early enough and the clinicians can not be exempt from blame for this delay in operation. There can not be a moment of doubt about the feasibility of operation when gastric dilatation is manifestly due to palpable neoplasm, even if it were not malignant. But we generally advise operation in case (1) dilatation is associated with cachexia; (2) absence of HC 1 in the gastric contents; (3) excess of lactic acid; (4) presence of the Oppler-Boas bacillus. Professor W. W. Keen, in quoting these deciding factors from this work (“ Phila. Med. Journal, ” vol. 1, p. 932), adds (5) when age is passed forty years ; (6) when hematemesis is present; (7) when examination of blood shows a diminution in red corpuscles and hemoglobin, and the digestive leukocytosis is absent. Stenotic symptoms, accompanied by these signs, are indications for operation, even in the absence of palpable tumor. Personally, I always urge operation when the first three conditions are persistently present and the case does not improve after three weeks of appropriate treatment. Exploratory laparotomy , which Haberkant states to be the only reliable means for making an early diagnosis of carcinoma, should be encouraged by the internist, not because carcinoma can be diag- nosed with certainty thereby, for it really can not, as the stomach is the seat of many kinds of neoplasms, and even ulcer, with indu- rated edges, may simulate carcinoma; so that the finding of a new HOW MANY PYLORIC NEOPLASMS ARE OPERABLE ? 357 growth does not include a knowledge of its exact nature, and if a carcinoma of small size be at the posterior side of the lesser curva- ture, it may escape attention even at autopsies until the stomach is removed from the body. The article quoted is an excellent piece of work, and the pessimistic view on the future development of clinical diagnosis need not discourage the clinician ; for the prog- ress which digestive physiology, pathology, and bacteriology have made in the last twenty years, and are still making, strengthens the belief that we shall, in the near future, be able to make early diagnoses of gastric neoplasms. Whether they will be operable or not is another question, which the clinician and the surgeon must investigate together. The practitioner should not be too guarded in advising explora- tory laparotomy in cases of rapidly developing cachexia and emaciation with the symptoms of chronic gastritis and absence of HC 1 . Tentative treatment should not be prolonged over three weeks. It is not near so serious a fault to have caused the opening of a stomach and found nothing operable, as to permit a case to continue and find out, at the autopsy only, that it was a circumscribed carcinoma the removal of which might have pro- longed life for years. The author has been responsible for three exploratory laparotomies at which nothing was found, although cancer was suspected in one and ulcer in the other two. The cases recovered and were cured of their symptoms, of pain and vomiting. One of these cases had vomited a pint of blood in the presence of the writer. At the operation, by Dr. J. M. T. Finney, nothing ab- normal could be found in the stomach. Even after the diagnosis is certain, much foresight is necessary in selecting cases for operation ; the establishment of the indication must be done with exactness and care. That the mortality from cancer resections has sunk from 65.4 per cent, in the period from 1879 to 1887 to 42.8 per cent, in the period from 1888 to 1894, and of benign stenosis from 42.8 per cent, to 27.7 per cent, in the same period, shows that the importance of exact “ Indicationsstellung ” is being appreciated. How many pyloric carcinomata are operable? In the records of the Vienna Pathological Institute, from 1817 to 1873, Gussenbauer and von Winiwarter found accounts of 542 pyloric cancers, of which 223 were entirely isolated, and 172 of these showed no adhesions; so 41. 1 per cent, were free from metastases, and 37.7 per cent, were, in addition to this, free from adhesions — the latter were suited for 35 8 SURGICAL TREATMENT OF ORGANIC GASTRIC DISEASES. resection. In many of the instances where the necropsy showed adhesions there must have been a time when they were not present ; so that a big field for operative therapy is opened. Streit found, at the Bern Pathological Institute, that 25.9 per cent. (“Deutsche Zeitschr. f. Chir.,” Bd. xvi) and Kramer (Konig, “ Lehrb. d. spec. Chir.,” Bd. 11) that 33.3 per cent, of pyloric cancers were operable. The best statistics state that from one-quarter to one-third of these neoplasms are operable. Adhesions increase the mortality ; in sixty-six cases of pylorectomy in which records were kept concern- ing this point, the mortality was 72.7 per cent, with, and 27.2 per cent, without, adhesions. No immediate recoveries are on record where there were adhesions of the pylorus with the transverse* colon, or with the colon and the pancreas together. Two patients with tumors of the curvatures and fundus, although distinctly ascertained to be malignant (they were causing no stenotic symp- toms ; so that the vicarious digestion of the intestines maintained the nitrogen equilibrium sufficiently), lived longer — not being operated — than two in whom gastro-enterostomy was performed. Both operated cases had adhesions. In the non-operated cases there were no adhesions found at autopsy — that is to say, the average duration of life after the date of exact diagnosis was longer in those cases of this type that were not operated than in those that were. Can the secretory and motor function be restored after total ex- tirpation of a malignant tumor? Obalinski and Jaworski(“ Wien. klin. Wochenschr.,” 1889, No. 5), Rosenheim (“ Deutsche med. Wochenschr.,” 1892, No. 49), Kansche (ibid.), and Zawadski and Sohnan (“ Deutsche med. Wochenschr.,” 1894, No. 8) assert that secretion is not restored by pylorectomy, but the last-mentioned authors assert that the motility may again become good. In cases that are operated before a complete de- struction of the gland-cells has taken place, the lost secretion of HC 1 has been observed to be restored. Rosenheim (“ Berlin, klin. Wochenschr.,” 1895, No. 1) and Boas (“ Deutsche med. Wochen- schr.,” 1895, No. 5) have reported the only two cases of this kind; so that it must be an extremely rare occurrence. Pyloric stenosis caused by simple benign adhesions can be re- moved by severing the constricting bands. These adhesions may cause pain and hematemesis without gastrectasia, as was shown in a case of Hahn’s (“Deutsche med. Wochenschr.,” 1894, No. 43), where laparotomy revealed five adhesions binding the stomach to the colon. He ligated each one of the strong bands doubly and GASTRO-ENTEROSTOMY VERSUS PYLORECTOMY. 359 severed it, and from that moment the patient recovered perfectly. Median herniae of the linea alba have been known to cause intense gastric suffering, necessitating operation. Rosenheim has described such cases, which were, however, much benefited by lavage and diet, so that the motor insufficiency was much improved (“ Berlin, klin. Wochenschr.,” 1897, No. 11). Preperitoneal lipomata have been known to cause interference with the motility and necessitate surgical interference. Adhesions may reunite after intersection and cause renewed trouble, as was shown in one case of Hahn’s, in which the adhesions were divided again by W. Levy two years after the first operation ; a few months after this Hadra executed a gastro-enterostomy, on Rosenheim’s suggestion (loc. cit.) f which gave no perfect relief, as the two previous operations had caused new adhesions. Referring again to malignant tumors of the lesser or greater curvatures where good motility is maintained, and that cases of this kind which are not operated may live a year or more, we might add the case of a lady in whom Musser and Da Costa diagnosed a palpable tumor in February, 1896. Personally, we determined the location in July, 1896, when there was complete loss of all secretion and numerous Oppler-Boas bacilli were present in the gastric contents. A fragment of the neoplasm was obtained in September, 1896, during lavage, clinching the diagnosis of car- cinoma. With daily lavage with HC 1 solution (4: 1000), highly nutritious and concentrated diet, rest, and internal use of HC 1 , condurango, and strychnin, this patient has gained twelve pounds in six months, and is still (September, 1897) able to take walks of two miles a day — nineteen months after Musser first diagnosed the existence of a gastric tumor.* The number of authoritative advocates of pylorectomy for benign stenosis is growing smaller and smaller. Von Hacker recently again emphasized that gastro-enterostomy is not used enough for the treatment of cicatricial stenoses of the pylorus and duodenum, and that it has the value of a radical operation for many cases with- out sharing its dangers (von Hacker, “ Magenoperationen,” etc., published by William Braumiiller, Wien, 1895). Mintz considers pylorectomy unjustifiable for benign cicatricial stenoses (“ Zeitschr. f. klin. Med.,” Bd. xxv). For mild stenotic cicatrices the pyloro- * This case lived eighteen months after establishment of diagnosis by the author. At one time, July, 1896, operation was strongly advised, but refused. The great difficulty with such cases is that the location of the tumor can not be determined with certainty. Exploratory laparotomy is safest for diagnosis. 360 SURGICAL TREATMENT OF ORGANIC GASTRIC DISEASES. plastic operation has proved sufficient. We shall refer to this opera- tion in the following : Atypical pylorectomy was executed first in 1885, by Billroth. It is a combination of resection of the pylorus with gastro-enteros- tomy recommended in cases where carcinomata, although operable, had so extensively involved the gastric walls that after resection it was impossible to suture the remainder of the stomach to the duo- denum, or where traction upon the duodenum to meet the stomach would produce too much tension upon the stitches. Von Eiselsberg executed the most extensive atypical resection of the pylorus in a very large but sharply limited carcinoma. His incision began close to the cardia and descended perpendicularly downward, so that only a small portion of the left fundus remained (“ von Langenbeck’s Archiv,” Bd. xxxix). Even this incision was not through healthy tissue, and the stitches tore through, termin- ating the case by perforation peritonitis. In twenty cases of atypical pylorectomy eight died — a mortality of forty per cent. The first case of immediate success by Billroth succumbed to a recurrence after four months. Kronlein performed this operation for traumatic cicatricial stenosis extending into the duodenum. Partial Pylorectomy and Partial Resections of the Gastric Walls . — The indications are given by the round ulcer, both on the anterior and posterior walls, cicatrices that produce interference, or tumors of the neighborhood that have extended to the gastric wall without involving the entire circumference of the pylorus. Partial pylorec- tomy preserves the valvula pylori, which is itself rarely the seat of gastric ulcer. In a total pylorectomy the sphincter and valve are removed entirely and replaced by a gradually contracting scar. Haberkant records eight such partial operations — three by Billroth (reported by von Hacker, loc. cit.), three by Czerny (“ Beitr. z. klin. Chir.,” Bd. ix, 1892), one by Spear (“ Centralbl. f. klin. Chir.,” 1885), and one by Schuchardt (Twenty-third German Sur- gical Congress, 1894). Billroth’s and Spear’s cases all died ; the three cases of Czerny recovered. The indications in the cases of the first two surgeons were: cicatrices, four times in the anterior pyloric wall. The indi- cations in the last three cases by Czerny were : ulcer, once ; exten- sion of sarcoma, twice. The case of stenosing ulcer, operated upon by the latter by this method, was still doing well, according to last reports, ten years after the operation. The case of Schuchardt’s is most instructive in bearing out our TOTAL GASTRECTOMY. 361 objection to Haberkant’s assertion that exploratory laparotomy is the only reliable means for early diagnosis of carcinoma. Schuch- ardt’s case had two open ulcers, only one of which was discov- ered when the stomach was opened, located at the lesser curvature and removed by excision of a piece as large as a 25-cent piece. Although no peritonitic symptoms appeared, death occurred under progressive cachexia in fourteen days. The necropsy showed a second, much larger ulcer, which, in Haberkant’s ( loc . cit. , p. 514) own words, was not only inoperable, but could not even be pal- pated. If a very large ulcer can not be palpated when the stomach is exposed, exploratory laparotomy is not infallible as a diagnostic method ; it may desert us like our clinical methods. The oldest resections of the gastric wall are by Billroth (“ Wien. med. Wochen- schr.,” 1881, p. 275) and Esmarch (quoted by Wolfler, loc. cit), for the repair of fistulae. Rupp resected a subserous leiomyoma of the anterior wall near the cardia in this way (“ von Langenbeck’s Arch.,” Bd. xl, p. 756). The number of partial resections, including both those of the pylorus and of the anterior gastric wall, amount to fifteen opera- tions ; eight were cured, seven were fatal, giving a mortality of 46.6 per cent. Total Gastrectomy. — In 1897 Schlatter reported the first com- plete gastrectomy anatomically proved as such (“ N. Y. Med. Rec.,” December 25, 1897, lii, 909). The operation was performed September 6, 1897. The patient lived one year and two months, dying October 29, 1 898. Death was due to multiple carcinomatous metastases, and was not ascribed to inanition. Brigham (“ Boston Med. and Surg. Jour.,” May 5, 1898) reported a complete removal of the entire stomach for carcinoma, and anastomosing the duodenum to the esophagus by the Murphy button. Brigham’s case was still doing well in June, 1899. MacDonald (“Jour. Am. Med. Assoc.,” September 3, 1898) and Richardson (“Boston Med. and Surg. Jour.,” October 20, 1898) have reported successful gas- trectomies. A case of gastrectomy reported by Summa and Ber- nays (“Jour. Am. Med. Assoc.,” February 12, 1898) died thirty-six hours after operation. W. W. Keen (loc. cit) concludes that abstention from such extensive operations is the wiser course to pursue. The author has already pointed out that nothing new has been added to our knowledge of the physiology of the stomach by Schlatter’s investigations (Hemmeter, “New York Med. Record,” liii, p. 409, March, 1898). That digestion and metabolism would 24 362 SURGICAL TREATMENT OF ORGANIC GASTRIC DISEASES. go on normally for a limited time in the absence of the stomach was known long before Schlatter’s operation. Gastro-enterostomy. — In the beginning of this chapter we described the various (three main) types of this operation that have been suggested. Which of these types of operation — Wolf- ler’s, von Hacker’s, Billroth-Brenner’s, or any of the other methods described in modern text-books on abdominal surgery — is to be selected is a matter to be decided by the surgeon. But we would remark in parenthesis that the physiological rotation of the full stomach around its long axis, whereby the large curvature is turned anteriorly and the smaller posteriorly, which is asserted by’Tiede- mann, has been confirmed by no other experimenter. Betz and Lesshaft (“Virchow’s Arch.,” 1882, vol. lxxxvii) have opposed the view. In many hundreds of experiments on the full stomachs of animals for the study of the peristalsis we have never observed it, and even if it were observed when the abdomen is opened, it could not then be considered physiological. The hypothetical gastric rotation has been adduced as an objection to Wolfler’s anterior antecolonic operation, on the ground that the artificial lumen between stomach and intestine was compressed by bring- ing the loop between the abdominal wall and the stomach dur- ing this rotation. Von Hacker’s method does avoid spur for- mation, and thereby retroflux of duodenal contents into the stomach, and also compression of the transverse colon by the in- serted jejunal loop. In addition to this the entire intestinal canal remains unchanged in its natural anatomical relations. Von Hacker himself states that the mortality is not materially reduced by his method. The functional results are claimed by most German sur- geons to be better with von Hacker’s operation. Chlumskij col- lected, in all, 550 gastro-enterostomies (“ Zeitschr. f. klin. Chir.,” 1898, xx, 231). According to his table, the mortality in 231 cases operated by the Wolfler method was 38.09 per cent.; of 152 cases by the von Hacker method, 32.52 per cent. In the latter method the escape of gastric contents into the intestine is facilitated by gravity. Results . — In 388 cases Haberkant found the total mortality to be 41.5 per cent. For gastro-enterostomy for carcinoma it was 43.5 per cent. ; for ulcer, 25.5 per cent. One of the indications of gastro- enterostomy is the simple atonic dilatation. Four such operations are reported, one of which (Selenkow) died and the remaining three (Renton,' von Kleef, and Jeannel) recovered and the func- PYLORO PLASTIC SURGERY. 363 tional result was good. Concerning the remote results, it is self- evident that in carcinoma they can not be of long duration, as the growth is left intact ; nevertheless the table at the end of this article shows ten cases in which the recovery lasted over a year. A sin- gular gastro-enterostomy is that reported by Hahn (“ Berlin, klin. Wochenschr.,” 1894, p. 1097). The operators were convinced that the neoplasm was a carcinoma ; the patient lived seven years after the operation without complaints, the tumor always being palpable. This case will always remain a doubtful one. Robert F. Weir has attempted to prove statistically that gastro- enterostomy keeps patients with pyloric carcinoma alive as long as pylorectomy, whereas the mortality is in the proportion of twelve per cent, for the former to fifty-two per cent, for pylorectomy. Haberkant’s statistics of a much larger number of cases show a mortality of 54.4 per cent, for resection to 43.5 per cent, for gas- tro-enterostomy. But then many cases have formerly been resected that would in the present advanced state of knowledge not have been operated. Pylorectomy gives a better prospect for more last- ing recovery than gastro-enterostomy. Of forty-seven cases recov- ered from pylorectomy, twenty-two lived longer than one year after the operation; but of fifty-eight cases of gastro-enterostomy, only twelve lived longer than one year. With the exception of Hahn’s doubtful case, there is no gastro-enterostomy in which the recovery lasted longer than two years ; but of Haberkant’s collected success- ful pylorectomies, twelve lived longer than two years. Pyloroplastic Surgery (Pyloroplasty). — This operation was first devised by von Heinecke, in March, 1886. The first operation was a success. In February, 1887, Mikulicz rediscovered and applied the method independently of von Heinecke. The opera- tion, which is applicable to some pyloric cicatrices, is carried out by slitting open the scars longitudinally in the line of the pyloric lumen and pulling the wound-edges apart by hooks inserted in the middle ; then they are reunited by sutures transversely. Graphi- cally, the procedure is expressed thus : Cases have been reported in which pyloroplastic surgery was attempted, and, failing, a pylorectomy had to be done (Lobker, 364 SURGICAL TREATMENT OF ORGANIC GASTRIC DISEASES. “ Verhandl. des XXI. Deutsch. Chir. Kongresses,” 1, 60). Czerny reported a case in which resection had to be done because the scar was so rigid it could not be unfolded (“ Beitrage z. klin. Chir.,” Bd. ix, 1892, p. 678). The cases that recover from a successful opera- tion of this kind are, as a rule, cured permanently ; no return of pyloric stenosis has been reported. Up to 1894 (inclusive), 5 1 operations of this type have been com- piled, 40 of which were successful and 11 fatal, making a mortality of 21.5 per cent. In 44 instances where the indication was stated, there were 7 peptic ulcers and 37 cicatricial stenoses ; but of these 37 scars, 14 were produced by corrosive poisons. The combined tables of Bavton and Bull (“New York Med. Rec.,” May 25 and June 8, 1889) contain 28 cases, with a mortality of 31.1 per cent. Digital Divulsion of the Pylorus. — Loreta’s operation consists of a simple gastrotomy and subsequent gradual expansion of the pylorus, by introducing first one and then two fingers ; the dilat- ing forceps has been used for the same purpose. Hahn recom- mended that the anterior wall of the stomach should be invaginated upon the finger and carried into the opening of the pylorus. The dangers of the procedure consist in (i) rupture or production of hemorrhages by lesions of the gastric wall, (2) frequent return of the stenosis. According to Bull (“ Centralbl. f. Chir.,” 1890, S. 149), Loreta himself has had the return occur in three cases. Haberkant ( loc . cit.) has compiled 31 cases of Loreta operations, with 19 cures and 12 deaths — a mortality of 38.7 per cent. Three of the fatal opera- tions were for carcinomata. Novara had to execute a resection after divulsion had failed ; the only justifiable indication is cicatricial stenosis. The operation has few advocates, and will have to give way to more exact and reliable operative methods. For atonic forms of dilatation that resist all medical treatment, Heinrich Bircher, of Aarau, Switzerland, has devised a new opera- tion, called g astro plication. This surgeon attempted to improve the motility of the stomach by a reduction of its size through making a fold or plait in the gastric wall. The greater curvature is raised to a much higher level by this operation. Bircher ob- tained good results in three cases, one of which, however, died three months after the operation. A certain amount of muscular tonicity must still be left in order to make this operation even a partial success (“American Jour. Med. Sciences,” 1892, vol. cm, p. 333). GASTROPEXY — GASTRO- ANASTOMOSIS. 365 The operation has not as yet been repeated in a sufficiently large number of cases to permit of a correct judgment of its real value. Weir (“ New York Med. Jour.,” July 9, 1892), unaware until two days before the operation that Bircher had preceded him, did a similar operation, but united the two layers of the gastric wall by four successive rows of interrupted silk sutures, the final one unit- ing the greater curvature to the lesser. Keen (Joe. cit) considers the technic of Weir a decided improvement over Birchers’.* Gastropexy is the name of an operation for the relief of gastro- ptosis, by suturing the stomach to the anterior abdominal wall. The stomach is not opened during the operation. Duret (“ Revue de Chir.,” 1896, xvi, 421) reports a successful case. Davis modi- fied the technic somewhat and reported two successful cases (“Western Med. Rev.,” Oct., 1897). Treves described a case of hepatoptosis, gastroptosis, and gen- eral enteroptosis brought about by adhesions of the omentum to old calcareous, tuberculous glands in the mesentery of the ileum and lying in the right iliac fossa. The glands were removed and the liver sewed firmly to fibrous tissues around the ensiform cartil- age. The adhesions of the omentum which had drawn the organs down were loosened, which, together with the hepatopexy, restored the stomach and colon to their places. The patient recovered en- tirely after having suffered for six years. Gastroplasty, gastro-anastomosis, and gastro-gastrostomy are operations for the relief of hour-glass stomach. Fifteen opera- tions of this kind have been done (W. W. Keen, loc. cit.). In two of them radical relief could not be given by the operation. Of the remaining thirteen cases, twelve were successful. Gastro-anastomosis is an operation first performed by Wolfler for hour-glass stomach, by which one portion of the organ is anas- tomosed with the other at the greater curvature. Gastro-anasto- mosis remedies the separation of the organ into two distinct cavities separated by a narrow isthmus. Von Hacker reports and pictures cases of hour-glass stomachs complicated with cicatricial pyloric * Professor Randolph Winslow, of the University of Maryland, executed a gastro- plication upon a well-known physician of Baltimore upon my advice. The patient was over sixty years of age, made a perfect recovery, and was well at date of revision, four months after operation. There had been motor insufficiency for five years and loss of secretion due to constant drain upon the secretory apparatus. The secretion of HC 1 was found to be equal to 20° — NaOH four months after operation. 10 366 SURGICAL TREATMENT OF ORGANIC GASTRIC DISEASES. stenosis, for which he recommends a double operation — either a pylorectomy, or a pyloroplastic operation with gastro-anastomosis, or, best, a gastro-enterostomy and gastro-anastomosis (von Hacker, “ Magenoperationen,” etc., Wien, 1895). The Fundamental Factors Influencing the Rate of Mor- tality in Gastric Operations.— These are partly under the control of the surgeon and partly not. Those over which we may exer- cise control are (I) defects in the technic, (II) selection of the kind of operation, (III) duration of the operation. The factors that escape control are (I) age of the fundamental disease, (II) nature and extent of this disease, (III) age of the patient. A. Factors Under the Control of the Surgeon. I. Faults in the technic , as a rule, lead to peritonitis, of which one must distinguish two kinds : ( a ) The septic, produced by infection during the operation; and (b) perforation peritonitis, due to a technical defect in placing the sutures. Perforation peritonitis as a result of insufficiency of the sutures is much more common in pylorectomy than in gastro-enterostomy, because the lines of suture are much longer. However, peritonitis may be caused by errors in diet or by spontaneous perforations in other parts of the stom- ach, independently of the technic. In 165 fatal cases with autop- sies, the cause of death was peritonitis in one-fourth of the cases; only three fatal cases were due to spontaneous peritonitis. II. The selection of the proper operation for any particular case is facilitated by an exact definition of the indications. The indications for pylorectomy are : (1) the operable carcinoma or sarcoma; (2) the peptic stenosing ulcer or cicatrix; (3) perfora- tion from pyloric ulcer. The contraindications are : (1) ( a ) Firm adhesions, especially posteriorly on account of dan- ger of injuring the hepatic artery and vein ; ( b ) adhesions with the pancreas, ( c ) with the liver, (d) with the meso- and transverse colon. (2) Infiltration of lymphatic glands ( a ) of the lesser omentum, ( b ) posterior surface of the stomach, (c) of the porta hepatis. (3) Icterus from metastases or compression by the tumor. (4) Great exhaustion of the patient. Severe gastric hemorrhage can be treated in most cases by inter- nal medication. Gastric ulcers that have given rise to repeated grave hemorrhages have been successfully excised by Czerny (“ Archiv f. klin. Chir.,” 1884), Cordua (quoted in Debove and Re- INDICATIONS FOR PYLORECTOMY AND GASTRO-ENTEROSTOMY. 367 mond, “Traite de Mai. de PEstomac ”), and Mikulicz (“ Deutsche med. Wochenschr.,” 1892). Dunin asserts that ulcers in the pyloric region causing serious hemorrhages would heal rapidly if the pyloric passage were put at rest by a gastro-enterostomy (Mintz, loc. cit). Kuster cured persistent hematemesis from pyloric ulcer on the posterior wall by opening the anterior wall, producing scabbing in- crustation with the thermocautery, and making a wide gastro-enter- ostomy. During the operation a cherry-stone was extracted from the depth of the ulcer. Mikulicz did a pyloroplastic operation for uncontrollable hemorrhage. The gastro-enterostomy, ^fter cica- trizing the ulcers with the thermocautery, is generally a prophy- lactic measure to forestall a prospective pyloric stenosis. A pyloro- plastic operation may accomplish the same object. For perforation of gastric ulcer many operations have been exe- cuted. Pariser has recently reported forty-three such operations, with thirty-three deaths and ten recoveries. Only in four cases was the perforation in the pylorus (Pariser, “ Deutsche med. Wochen- schr.,” 1895). N. Senn suggested gastric distention with hydrogen, in order to rapidly find out the seat of the perforation. Indications for gastro-enterostomy : (1) Pyloric carcinoma with extensive adhesions and glandular metastases. Frequently it is not decided to do a gastro-enteros- tomy until the abdomen is opened; a resection has often been planned, but had to be replaced by a gastro-enterostomy. If the posterior wall alone is free from infiltration, von Hacker’s method is indicated ; in the reverse case, the methods of Wolfler or Billroth- Brenner. (2) Stenosing ulcer ( a ), both when the pylorus is still isolated and free, and ( b ) when it is adherent to its surroundings. With this indication pylorectomy is unjustifiable, but partial resection and pyloroplastic surgery may yet compete with gastro-enteros- tomy. When, however, a cicatricial pyloric stenosis extends into the duodenum, nothing but a gastro-enterostomy should be done. (3) Stenoses in the duodenum outside of the pylorus. Four operations, with three recoveries, have so far been executed for this indication. (4) Stenoses by neoplasms of neighboring organs — the gall- bladder, periportal lymphatic glands, and pancreas. Novarro per- formed a gastro-enterostomy for pyloric stenosis caused by echino- coccus cyst of the liver (“ Deutsche med. Wochenschr.,” 1891, No. 368 SURGICAL TREATMENT OF ORGANIC GASTRIC DISEASES. 4, S. 152). Stansfield did the same operation, with good result, for tumor of the pancreas (“ Brit. Med. Jour.,” 1890, pp. 294 and 1300), making use of Senn’s bone-plates. (5) Purely functional dilatation due to atony of the musculature without pyloric stricture. Four gastro-enterostomies for this indi- cation are on record. Gastroplication (resection or reduplication of a fold of the stomach-wall) is preferable for this purpose. III. The Duration of Gastric Operations . — It is evident that the sooner an operation is completed, the less the danger of shock and sepsis. With the view of shortening the time of operation, Rydy- gier and Lauenstein advised the employment of continued sutures, which they claim abbreviate the time by one hour. The most celebrated time- and labor-saving devices in gastro-intestinal sur- gery are by our countrymen, Murphy and Senn. The advocates of Senn’s bone-plates have claimed that the mortality under the older suture methods was from 42.8 per cent, to 47 per cent. (Her- bert Page and von Hacker), and in forty-one operations by the Senn method the mortality was only 24.5 per cent. The decalcified bone-plates of Senn are not always digested. In one of the inventor’s own cases they were vomited undigested forty hours after the operation. Haberkant asserts that the advantage of the saving of time is counterbalanced by less safety. For surgi- cal opinions on the Murphy button and Senn plates we must refer to journals and text-bpoks on abdominal surgery. But so much is clear : shortening of the time of operations by these contrivances is a great gain. B. Factors that Escape Control. I. Age of the Underlying Disease. — This can not be determined statistically, for both ulcer and carcinoma may remain latent for months, and it is impossible to ascertain the age of these conditions at the autopsy. We have observed a large carcinoma in a white woman who died at Bay View Hospital. The neoplasm occupied the posterior gastric wall ; during life there had been no gastric symptoms whatever. Osier’s case of very rapid course in gastric carcinoma — two weeks from the onset of severe dyspeptic symp- toms — made it plain at the autopsy that the growth had been of considerable duration, but had for a long time not undermined the patient’s health (“Univ. Medical Magazine,” January, 1895). The anamnesis given by patients regarding the period since when they have suffered from dyspepsia is frequently unreliable. II. Nature and Extent of the Fundamental Gastric Disease. — Con- EFFECT OF AGE ON THE OPERATIVE RESULTS. 369 cerning this point the statistics show that the mortality in pylo- rectomy, as well as in gastro-enterostomy, is greater for carcinoma than for ulcer. Under the head of contraindications to these operations we have dwelt upon the dangerous influences of the extent of the disease. III. Effect of the Age of the Patient . — In the cases as they are pre- sented for operation there are so many other governing factors that the matter of age does not appear, from statistics, to exert much influence on the result of these operations, provided the other conditions previously mentioned are favorable. A difference becomes noticeable when the age is over sixty years. Among 176 resections, the percentage of mortality of those under fifty years was 50.4 per cent., and those over fifty years, 52.9 per cent. With gastro-enterostomy the rate was 42.4 per cent, for those under fifty years, and 57.7 per cent, for those over fifty. These statistics, therefore, do not confirm a marked influence of age on the rate of mortality. A critical consideration of these factors, in connection with other elements before mentioned, justifies the hope that diagnosis and gastric surgery have not reached the highest development as yet, and we may expect a further lowering of the rate of mortality. An artificial communication between the stomach and intestines, as is performed in gastro-enterostomy, may become much smaller by cicatricial contraction. Kocher has reported two such observa- tions. In one case Czerny made an opening three cm. in diameter ; at the autopsy, five months later, it had contracted down to eight mm. Heinsheimer has made careful analytical observations on the metabolism in two cases of gastro-enterostomy (“ Mittheilungen a. d. Grenzgebieten d. Medizin u. Chirurg,” Bd. 1, S. 350). In this piece of work, which was done under von Noorden, Rachford’s ob- servation that fats require a very thorough and intense mixture with the secretions of the pancreas and liver for their digestion (“ Centralbl. f. Phys.,” 1896, Heft 4) was confirmed. The further away the gastro-intestinal communication is laid from the duodenal orifices of these glands, the more defective the fat digestion and resorption. It is therefore suggested that in gastro-enterostomies a jejunal loop, as near as possible to the duodenum, be anastomosed with the stomach. For benign stenoses of the pylorus, pylorectomy is more and more deserted in favor of gastro-enterostomy, which gives the 370 SURGICAL TREATMENT OF ORGANIC GASTRIC DISEASES. same functional results without the dangers (Ernst Siegel, “ Mit- theil. a. d. Grenzgebieten d. Medizin u. Chir.” Bd. i, S. 347). DURATION OF LIFE AFTER RESECTION IN 51 CASES OF CARCINOMA OF PYLORUS. — {Haberkant . ) Death. Number of Cases. Causes of Death. Living at Date of this Report. Number of Cases. After I y z months, Return of cancer. After 2 months, I “2 “ 3 One of metastasis in the “ 3 “ I liver. . “ 3/2 “ ] 2 K 1 Acute lung disease, no re- “ 4 “ r turn and no metastasis. “ 6 “ I “ 4 2 Return. “ 7/2 “ I “ 5 2 One of lobular pneumonia. “ 8 “ I one of chronic pyemia. “ 9 “ I “6 “ 2 One of return, one of “ I year, 2 cicatricial stenosis. “ 1 year and “ 6^ - 1 Return. 2 months, I “ 7 2 “ i)4 years, I “ 8 1 Return. “ 2 “ 2 “ 10 “ 1 Return. “ 2 years and “ 11 X “ 1 Rectal and pelvic carci- 2 months, 2 noma. “ 2)4 years, I “ 1 year, . . 3 Two return. ‘ ‘ a 1 m 0 s t 3 “ 13 months, 2 Return. years, I “ iy years, 1 Return. “ 3 >2 years, I “ 2 K “ 1 ‘ ‘ 5 years and “ 3 1 Cicatricial stenosis. 4 months, I Kocher. “ SJ 4 “ i Not stated (Billroth). Over 8 years, I Ratimmow. Total, . . 26 Total, . . 21 RECOVERIES AND DEATHS: PERCENTAGE OF MORTALITY IN 379 CASES OF RESECTION OF PYLORUS .—(Haberkant.) Year of Oper- ation. Name of Operator. Number Operated Upon. | Result Carci- noma. Ulcer and Cica- tricial Steno- sis. Sar- coma and Myoma. NoIndi- CATION Stated. Remarks. Recovered. 'U 5 Recovered. T3 893 Roux, . . . 5 3 2 3 2 One atypical, the rest typical, total resections. 1893 Doyen, . . 7 6 1 2 1 4 All atypical pylorec- tomies. 1893 Lobker, . . 13 7 6 5 5 2 1 1893 Schede, . . 13 7 6 6 5 1 1 1893 von Kleef, . 4 3 1 3 1894 Kraske, . . 4 1 3 1 3 I894 Czerny, . . 20 13 7 8 5 3 2 2 Three partial resec- tions, the rest typ- Sar- ical, total pylorec- coma tomies. 1894 Kocher, = . 9 7 2 7 2 In all nine cases Kocher used his method with fol- lowing gastroduo- denostomy. Kronlein, 8 5 3 5 3 I894 Kappeler, . 14 9 5 8 5 1 Total mortality, 35 7 per cent. For car- cinoma alone, 38. 1 per Cent. £ 00 Mikulicz, Other cases, 20 i 5 5 13 5 2 exclusive of above, . . 166 79 87 60 76 8 6 2 9 5 Of these, 147 were total resections ; 17 atypical, and 2 1 Angi- oma fi- brosu'm . partial pylorecto- 1 Lym- phosar- mies. coma. Total, . . . 379 191 i I *88 130 i 45 32 ’20 5 24 23 RESULTS WITH GASTRO-ENTEROSTOMY FROM 1885 TO 1893. Year of Publica- tion. Author. Number of Opera- tions. Result. Total Mortality. Per Cent. Carcinoma. Ulcer and Cicatricial Stenosis. Recovered. Died. Recovered. Died. Mortality. Per cent. Recovered. Died. Mortality. Per cent. 1885 Kramer, .... 20 8 12 5 II 68.7 3 I 1886 Saltzmann, . . . 2 3 0 12 66.6 1887 Rockwitz, . . . 29 16 13 44.8 11 12 5 I 1890 Novarro, .... 55 24 43 - 6 1890 Meliler, .... 55-1 58.8 38.5 1891 Page, 3 6 15 41.6 1892 Hadra, .... 76 33 43 56 1893 Zeller, 152 86 66 43 4 39 i 24 64 141 144 8 2 RESULTS OF VARIOUS OPERATORS WITH GASTRO-ENTEROSTOMY.— ( Haber kant .) Year of Publica- tion. Operator. Number of Cases Oper- ated Upon. Carci- noma. Ulcer and Cica- tricial Sten- osis. Dilata- tion of the Stom- ach. Sar- coma. No Indi- cation Stated. Remarks. Recovered.! -d 5 Recovered. 5 Recovered. -6 5 Recovered. r o IU s Recovered T 3 5 1887 Liicke, . . 8 5 I 2 1890 Billroth, . . 28 14 14 1890 Novarro, . . IO 5 3 2 1891 Lauenstein,. 17 10 3 2 2 1891 Hahn, . . . II 5 6 1891 Bowreman - Jesset, . . 5 3 2 1891 Senn, . . . 13 4 9 Calculated according to Czerny. 1891 Remedi, . . 6 3 3 1893 Roux, . . . 14 7 7 1893 Doyen, . . 10 6 4 Two carcinomata, eight cicatrices. 1893 von Kleef, . 19 I . ■3 5 1893 Cordivilla, . 6 2 4 Operated in one year by von Hacker’s method. 1893 v. Heinecke, 6 4 2 1893 Lobker, . . 7 4 3 All according to von Hacker’s method. 1894 Czerny, . . 23 12 7 2 1 I 1894 Kraske, . . 10 7 3 Other cases, exclusive of above, . . 195 66 59 20 9 2 1 1 ; 21 16 Total, . . 388 136 105 35 12 3 1 ■ 1 52 42 3 72 OPERATIVE STATISTICS. 373 DURATION OF LIFE AFTER GASTRO-ENTEROSTOM Y. Death. Number OF Cases. Living and at the Time of Report in Good Health. Number of Cases. After I month, 8 After 2 months, ... j “ I months, i “3 “ 2 “2 “ 5 “ 4 “ • ••• I “2^ “ 2 “ 5 “ • • • 2 “3 “ 4 “6 “ 2 “ 3 l A “ 2 “7 “ 2 “4 “ ... . 5 “ S/z “ I “6 “ 3 “9 “ 2 “ 7 'A “ ... i “ 10 “ I “ IO “ i “ 1 year and 11 months, . I “ I year, 3 “ 2 years, I (Hahn). “ i year and 2 months, . . i “ years, 3 “ I year and 7 months, . . i “ I “ “ 8 “ i “ I “ “ IO “ i Total, 42 Total, 16 EFFECT OF AGE ON THE RESULT OF VARIOUS GASTRIC OPERA- TIONS. — ( Haberkant . ) Age. Total Typical Resection of Pylorus. Gastro-enteros- TOMY. Atypical Resec- tion of Pylorus. Pyloroplastic Operation. Number of Operations. Recovered. Died. Number of Operations. Recovered. Died. Number of Operations. Recovered. Died. Number of Operations. Recovered. Died. 20 years. 2 2 I I 2 2 22-30' “ 9 6 3 21 14 7 3 I 2 5 2 3 31-40 “ 44 21 2 3 47 26 21 2 2 IO 7 3 41-50 “ 70 33 37 37 21 16 3 2 I 5 4 1 51-60 “ 37 20 17 33 l6 17 1 I 3 3 61-70 “ 13 4 9 11 2 9 Over 70 “ 1 1 1 1 1 1 uo ( 73 ) 374 INFLUENCE OF GASTRIC DISEASES UPON OTHER ORGANS. CHAPTER VIII. INFLUENCE OF GASTRIC DISEASES UPON OTHER ORGANS AND ON METABOLISM. Diseases of the stomach may, as is well known, affect general nutrition, the action of the heart, lungs, and the nervous system. In all digestive diseases with apparent malnutrition the physi- cian should ascertain the amount and the kind of food ingested, the state of the stool, and sleep. The cause of insufficient inges- tion of food is anorexia in the majority of cases ; in others the patients have a good appetite, but avoid food because it gives them pain, as in the case of gastric ulcer; others, again, will not eat because they vomit the food soon after ingestion. Loss of weight is of more serious significance in chronic than in acute stomach diseases. Instead of taking in thirty to forty calories per kilogram of body weight, von Noorden found in chronic types, after careful observation, that they ingested only twenty-one calories of their own accord (v. Noorden, “ Ueber Stoffwechsel d. Magenkranken,” etc., “ Berliner Klinik,” Heft 55). In cases in which the HC 1 secre- tion was so diminished that only a fraction of the proteids could be peptonized in the stomach and the largest portion passed into the intestines unchanged, von Noorden found that resorption of the main food-substances was sufficient. With a good gastric peris- talsis, preventing delay and fermentation in the stomach, the intes- tine is capable of supplanting the deficient gastric digestion. In animals, total exclusion of the stomach from the digestive act need not injure general nutrition, provided the food is supplied in a proper form. It is very probable that in certain forms of gastritis, in ectasias and carcinoma, poisonous substances are formed which are re- sorbed and injure the metabolism of the tissues. Friedenwald has recently found this to be the case in atony of the intestines and stomach (“ Med. News,.” Dec. 23, 1893). Resorbable and combustible gases are developed in gastrectasias with stagnating ingesta and have been described by many observers (see Albu, “ Die Autointoxicationen des Intestinaltractus,” p. 19). . Putrefaction of albuminous substances may occur in the stomach. Some cases show the formation of sulphuretted hydrogen even INFLUENCE OF GASTRIC DISEASES ON THE HEART. 375 with co-existent high acidity. Naturally, stagnation must be present to make albuminous decomposition possible. Muller has described a series of carcinoma cases in which more nitrogen was ex- creted than ingested in the food (“ Zeitschr. f. klin. Med.,” Bd. xvi), which strengthens the conception of carcinomatous auto-intoxica- tion, causing an increased albuminous breakdown in the tissues. In all cases of subnormal nutrition all etiological factors must be sought out, and an individualized, highly nutritious, concen- trated, unirritating diet adapted to the patient after improving the appetite.* Influence of Gastric Diseases on the Heart. — It is natural to expect increased rapidity of the heart’s action in all gastric diseases associated with fever, such as the various forms of acute gastritis, in perigastritis, and other complications (peritonitis). But tachy- cardia has frequently been observed by us associated with hyper- acidity, gastrosuccorrhea, and pneumatosis. In one case of the latter disease the tachycardia was so persistent as to require special treatment by local ice-bag, aconite, and bromid of strontium. In all of these cases fever was absent, and we have no experimental basis to explain the phenomenon. Bradycardia is seen much more frequently, and the fact that it is aggravated and improves or disappears as the gastric trouble becomes worse or better, shows that it is not an accidental accom- paniment, but is in some causal relation with the fundamental disease — i. e ., dilatation or ulcer. In animals, slowing of the pulse can be effected by distention or rough manipulation of the stomach. Stimulation of sensory nerves causes slowing of the heart-beat, and this may partly be offered as an explanation of bradycardia in dilatation and ulcer, though it is far from satis- factory. It is difficult to prove that irregular heart’s action or arrhythmia is dependent upon gastric diseases, even when it actually is associated with the latter. Arrhythmia is so frequent that it may accidentally be present in an individual independently of any gas- tric disease. Patients with weak hearts, valvular disease, failure of compensa- tion, should be carefully dieted, and, if in extreme dyspnea, should not be allowed anything but milk until this symptom is relieved. *The literature on the correlation of digestive diseases and those of other organs, and vice versa, will be found in Dr. Hans Herz’s “ Storungen des Verdauungsapparates als Ursache u. Folge anderer Erlcrankungen,” Berlin, 1898. 376 INFLUENCE OF GASTRIC DISEASES UPON OTHER ORGANS. Arrhythmia and compensatory defects are more pronounced after full meals. The relation is not perfectly clear ; but we have ob- served a number of deaths in patients suffering from organic cardiac disease, following shortly after a full meal that was apparently en- joyed. These deaths may be attributed to a number of causes — viz. : (1) Impediment offered to excursions of the diaphragm by the full stomach ; (2) pressure on the weak heart, and irritation of the pneumogastric nerve, due to distention of the stomach by gases; (3) absorption of toxins from improperly digested food ; (4) increased intracardiac pressure occurring naturally during gastric digestion. When the heart is dilated or hypertrophied, very small meals only should be permitted. Palpitation of the heart occurs in many persons, particularly after heavy meals ; the pulse becomes faster, fuller ; the tension greater — all this with intact hearts, but particularly observable in the course of chronic gastric diseases, dilatations, abdominal plethora, and constipation. Respiration. — It is undoubted that breathing is influenced by gastric troubles, although sufficient attention has not been given to this matter. We have noticed in a number of cases that the respiratory expansion is lessened by gastric diseases impeding the excursions of the diaphragm. This we have produced experimentally in healthy individuals by inflating our stomach-shaped intragastric rubber bag within their stomach while they were under narcosis. It appears, therefore, that undue or excessive gastric distention diminishes the amount of inspired air, independently of conscious- ness. In gastric fermentations toxic substances are produced, which, when injected into the circulation, caused dyspneic respira- tion of a paroxysmal character (Bouchard and Bouveret). It is probable, therefore, that gastric diseases may affect respiration either directly or mechanically, through interference with the descent of the diaphragm or by the absorption of toxins and action on the respiratory center. With the intimate, mutual correlation of the physiology of the circulatory and respiratory function, it is evident that a pathological disturbance of one will inevitably affect the other. The Influence of Gastric Diseases on the Nervous System. — Nervous patients affected with a disease of the stomach fre- quently exhibit neuroses of sensation : hyperesthesia, intercostal neuralgias, and hemicrania. That there is some etiological con- nection between the stomach and these conditions is. made very From THE MEDICAL RECORD, New York, 44 The reproach that the English language can boast of no treatise on anatomy deserving to be ranked with the masterly works of Henle, Luschka, Hyrtl, and others, is fast losing its force. During the past few years several works of great merit have appeared, and among these Morris' 4 Anatomy' seems destined to take the first place in disputing the palm in ana- tomical fields with the German classics. The nomen- clature, arrangement, and entire general character resemble strongly those of the above-mentioned hand- books, while in the beauty and profuseness of its illustrations it surpasses them. This edition offers but few changes ; a chapter on the skin has been added, and a useful list of vestigial and abnormal structures has been compiled. Sections especially worthy of praise are those on surgical and topographical anat- omy, and the chapter on the nervous system is pre- sented with great clearness and fullness. The ever- growing popularity of the book with teachers and students is an index of its value, and it may safely be recommended to all interested." From THE PHILADELPHIA MEDICAL JOURNAL. Of all the text-books of moderate size on human anatomy in the English language, Morris is undoubt- edly the most up-to-date and accurate. The changes from the first edition are not marked; perhaps the most noticeable feature is that there are twenty less cuts than in the first edition. Those which have been omitted, however, will not be greatly missed. The saving of space by the omission of a discussion of histology is a decided advantage, giving room for much matter of importance in these days when every student is obliged to own a special treatise on histology. To enumerate the numerous differences which are noticeable in the descriptions given by this book from those in many of the older anatomies would require too much space. The changes, how- ever, almost without exception, tend toward an im- proved nomenclature and greater accuracy. This is particularly noticeable in the parts devoted to descrip- tions of the abdominal viscera and the joints. ♦ . . For the student, the surgeon, or for the general prac- titioner who desires to review His anatomy, Morris is decidedly the book to buy/ r MORRIS' ANATOMY* Second Edition. 790 Illustrations, of which over 200 are in Colors. Human Anatomy. A Complete Systematic Treatise by Various Authors, Including Special Sections on Surgical and Topographical Anatomy, the Skin, and Vestigial and Abnormal Structures. Edited by Henry Morris, M.A. and M.B. (Lond.), F.R.C.S., Senior Surgeon to Middlesex Hospital ; Examiner In Surgery, University of London; Member of the Council, and Chairman of the Court of Examiners, Royal College of Surgeons, etc. Second Edition. Rewritten in Parts and thoroughly revised throughout. With 790 Illus- trations, the greater part of which are Original, over 200 being printed In Colors. Royal Octavo. 1274 pages. Cloth, $6.00 ; Leather, $7.00 ; Half Russia, $8.00 Morris' “Anatomy ** was published at a time when methods of teaching , the art of engraving, and distinct advance in anatomical illustration made desirable a new and modem text-book* The rapid sale of the first edition, its immediate adoption as a text-book by a large number of medical schools, and its purchase by physicians and surgeons proved its value and made it from the day of publi- cation a standard authority. In making this new edition the editors and publishers have used every endeavor to enhance its value. The text has been thoroughly revised and in many parts rewritten; the editor has devoted himself to the task of making it a harmonious whole; many new illustrations have replaced those used in the first edition, and a large number have been printed in colors, while the typo- graphical appearance has been improved in several particulars. The illustrations, in number, correctness, and excellence of execution, are equaled by no similar treatise; about $1000 having been expended on new and improved blocks for this edition alone. P. BLAKISTON’S SON & CO., PUBLISHERS, 5012 WALNUT STREET, PHILADELPHIA. GASTRIC VERTIGO. 377 probable by the fact that very frequently they only occur after full meals (dinner), or, if they existed before, they are aggravated by copious eating, and become ameliorated or disappear as digestion is completed. The pains often return toward night and on going to bed, causing insomnia. Patients that are experienced in the use of the stomach-tube are able to arrest these pains at times by lavage. Occasionally, the colon is the cause of the pain irradia- tion ; this is especially to be looked for in membranous colitis or compression of the colon from tight lacing, or in the various forms of enteroptosis. Gastric vertigo is a form of dizziness or partial unconsciousness without pain, but frequently with nausea and vomiting, occurring in gastric sufferers. Trousseau, who gave a classical description of this affection, argued that one of its peculiarities was that con- sciousness remained clear during the attack (Trousseau, “ Clin, del’ Hotel Dieu,” Paris, tome in, 1868). Leube and Trousseau were of the opinion that it occurred most frequently with chronic gastritis. Boas and Herz consider that myasthenia is the most frequent substratum. We have observed transient loss of consciousness which at times developed from typical stomach vertigo. This affection occurs, in our experience, in neuropathic patients with hyperacidity, particu- larly when the stomach is empty, and is associated more often with this gastric neurosis than others. It is a more frequent complication of hyperchylia than is gener- ally known, since many patients will not speak of their transient attacks unless especially questioned. Emesis often checks the attack, and Trousseau mentions that a cup of bouillon or a cake soaked in wine may check the vertigo. Treatment of the fundamental gastric disease removes the vertigo, as a rule, but in explanation of the way in which the ver- tigo is caused, its nervous mechanism, etc., we have nothing but hypotheses. Symptoms . — The symptoms accompanying gastric vertigo are nausea, eructation, pyrosis, vomiting, sensitiveness in the epigastric region, pain in the stomach, and a feeling of pressure, fullness, and distention. In the majority of cases constipation exists, and the abdomen is frequently distended with gases. In some few cases a dilatation was found to be present. Vertigo has been observed to occur almost at any stage of digestion — before, during, and after meals. Sometimes the attacks of giddiness are announced by a 25 37§ INFLUENCE OF GASTRIC DISEASES ON THE NERVOUS SYSTEM. sensation of great hunger or bulimia. Leube mentions that gastric vertigo may occur in some persons after the ingestion of certain foods. It may occur either at intervals of several days or several times in the same day. It is generally a chronic and permanent trouble, but in its lighter forms it has no serious influence on the condition of the patient. The treatment of gastric vertigo necessi- tates the treatment of the underlying condition of the stomach. Leube has described an intestinal vertigo associated with intes- tinal diseases of various kinds, but generally not of a serious char- acter. The most frequent causes are constipation and intestinal parasites, mainly lumbricoid and tape-worms. These attacks of gastric vertigo are as yet not satisfactorily explained. Leube has in some cases been able to produce the attack by pressure on the stomach or intestines (Leube, “ Ueber den Magenschwindel ” ; Ziemssen’s “ Handb. d. spec. Path. u. Ther.,” vol. n, p. 66). Mayer and Pribram claim to have observed excitation of the vasomotor center after irritation of the stomach, particularly of the serous coat (Mayer and Pribram, “ Ueber reflect. Bezieh. d. Magens z. d. In- nervationscentren f. d. Kreislaufsorg.,” “Sitzungsber. d. Wien. Akad. d. Wiss.,” 1872). A second theory in explanation of stomach vertigo presumes that it is caused by cerebral anemia, or hyperemia, which is not described as a reflex act, but as a direct detrimental influence on the circulation of the brain. This hypothesis exag- gerates the degrees of circulatory variation that can possibly occur in such light forms of digestive disturbance in which vertigo is observed. A third theory explains gastric vertigo on the basis of auto-intoxication. It is presumed that products of abnormal diges- tion, which collect when the motor function of the stomach and intestines is disturbed, are absorbed into the circulation, and act directly upon the brain. There is an abundance of experimental evidence, as well as clinical experience, which proves that such an effect of toxic chemical substances is possible. Such toxic irrita- tion may be indirect, and is intermediated through the vasomotor center. Brieger has isolated a substance from dilated stomachs which he has termed peptotoxin, which has an extremely poisonous effect when injected into the circulation of animals. In case of the presence of intestinal parasites, the toxic metabolic products of the helminthiasis are added to those of disturbed digestive function. Rosenbach has demonstrated that there is a regulatory apparatus for the body movements and for equilibrium in the epigastric re- gion. This center distinctly enters into function when tests are TETANY OF GASTRIC ORIGIN. 379 made with eyes closed. This observation, if confirmed, would per- mit of new insight into the pathology of gastric vertigo. For, if this abdominal regulatory apparatus receives abnormal impulses, it is plausible that they may be conducted to the cerebrum by way of the sympathetic system. Tetany. — The term signifies characteristic convulsive attacks which occur in the course of gastric diseases, particularly in dila- tations associated with hypersecretion. The term “ tetany ” was first used in 1852 by Corvisart. The spasms are prevailingly tonic contractions, alternating with less severe twitchings in the flexor muscles of the arms, calves, and generally also of the abdominal muscles. The facial, cervical, and maxillary muscles are occasion- ally attacked by the tetany, the eyes may be turned upward, and even emprosthotonos of short duration has been reported. The convulsions may be painful and consciousness may be clear or completely obscured. In one case of Kussmaul’s the power of speech was lost ; in another the patient spoke disconnectedly and his pupils did not react to light. In a third the symptoms referring to the cerebrum were absent, but a fourth case of Kuss- maul’s was of an epileptic form and character. Bouveret and Devic (“ Rech. clin. et experim. sur la tetanie d’origine gastrique,” “ Revue de Medec.,” 1892, 12, p. 48) have collected twenty three cases of these tetanic attacks, and Albu (“ Autointoxicationen des Intestinaltractus,” Berlin, 1895) states that not more than thirty-six cases of this complication of gastric diseases have been reported. Kussmaul gave the first classical description of these attacks in his famous publication on the treatment of gastric dilatations by a new method by means of the stomach-pump (“ Deutsches Archiv f. klin. Med.,” Bd. vi). Clinically, it is not correct to designate all tonic muscular con- vulsions of gastric origin as tetany. In true gastric tetany there is an increased mechanical excitability of the muscles, and an in- creased mechanical and electrical irritability of the motor and sen- sory nerves, which precede the attack and may persist long after it. Cases have been reported by Fleiner and Kussmaul which strongly resembled typical tetanus. Cases are reported in which the clinical picture varied between tetany, tetanus, and epileptiform convul- sions. In most of the cases Trousseau’s phenomenon — i. e., the production of spasms by pressure on the nerve-trunks — was present. Among twenty-seven cases that were collected by Riegel, sixteen proved fatal. According to this, tetany is a very grave complica- 380 TETANY CAUSED BY AUTO-INTOXICATION. tion of gastric diseases. The gastric diseases with which tetany is associated are extensive dilatations, due mostly to stenosis of the pylorus or duodenum, by ulcer or cicatrix. In several cases the stenosis was due to a carcinoma that had developed from a cica- trix. Bouveret and Devic attribute great importance to hyper- secretion for the production of tetany. This complication has, however, been observed in other dilatations in which there was no hypersecretion. Thus far three hypotheses have been put forward attempting to explain the origin of tetany: (i) That of Kussmaul, according to which it is caused by desiccation of the organism in. consequence of copious loss of water. (2) The explanation accord- ing to which tetany is caused by a reflex irritation of the central and peripheral nervous systems, and that the irritation issued from the central branches of the gastro-intestinal tract. (3) That of auto-intoxication. Kussmaul’s theory rested upon the apparent analogy between tetany and the cramps in the legs occurring with Asiatic cholera, which are believed to be due to condensation and thickening of the blood resulting from loss of water. We know, however, that these cramps occur also in cholera sicca. The loss of water, Kussmaul thought, was brought about by the exhaustive vomiting which usually precedes the attack of tetany, but cases have been reported in which tetany occurred without a preliminary attack of vomiting. In cholera nostras (the acute gastro-enteritis of chil- dren), where the loss of water is very great, tetany occurs very rarely. Blazicek described a case of gastric tetany in which the percent- age of water in the blood was not reduced. The second theory, that of the reflex origin, has been proposed by Germain See. The arguments of Bouveret and Devic, and of Ewald (“ Berlin, klin. Wochenschr.,” 1894, No. 2), emphasize the fact that the reflex phenomena are based upon a preliminary chronic intoxication, which increases the irritability of the muscles and nerves. Tetany, according to these authors, is, therefore, not a reflex phenomena, any more than are the convulsions of a strych- ninized frog, which result from the slightest cutaneous irritation. Most modern authors (Gerhardt, Bouveret and Devic, Albu, Ewald, Heim, Loeb, Schlesinger, and Baginsky) favor an explana- tion of tetany on the basis of gastro-intestinal auto-intoxication. It is not a bacterial intoxication caused by metabolic products of pathogenic bacteria introduced with the food which these authors DYSPEPTIC ASTHMA. 3 « have reference to, but to poisons formed in the stagnating, ferment- ing contents of the dilated stomach. Kulneff has extracted toxic products from the gastric contents in carcinoma and dilatation, which, according to their chemical structure, were classed as dia- mins. These toxins were extracted by Brieger’s method (extrac- tion with alcohol and precipitation with mercuric chlorid). Bouveret and Devic extracted substances from the stomachs of three cases of tetany with hyperchlorhydria that produced spasms when in- jected into animals. Evvald and Jacobson have isolated alkaloidal bodies from the urine of tetany patients, and Albu isolated the double platinic and gold salt of an alkaloidal substance from the urine of a woman afflicted with tetany. This substance was absent from the urine when the patient was free from the attacks. Tetany occurs, in the majority of cases, only when abnormal fermentations and putrefactions occur in the stagnated contents of the stomach and intestines. This intoxication theory explains the nephritis which Loeb has observed in connection with tetany. The author has reported three cases of nephritis which probably owe their origin to auto-intoxication (Hemmeter, “ Maryland Med. Jour.,” July 24 and 31, and Aug. 7, 1897). The subject is not sufficiently investigated to permit of definite conclusions regarding the causa- tion. Asthma Dyspepticum. — In 1876 Henoch described a clinical phenomenon in children, in which attacks very similar to asthma were associated with digestive disturbances (Henoch, “ Berlin, klin. Wochenschr.,” 1876, No. 18), and in 1882 Silbermann de- scribed similar cases, also occurring in children (“ Berlin, klin. Wochenschr.,” 1882, No. 23). The attacks of asthma dyspepticum are characterized by a very abrupt, acute onset, after a very evident error in diet or after constipation or febrile gastritis. There is a pronounced dyspnea, with cyanosis, very small, compressible, and hurried pulse, cold extremities, collapse, and, generally, no symp- toms of severe gastric disturbance. The symptoms disappear as suddenly as they begin, after an emetic has taken effect or spon- taneous vomiting has occurred. Strumpell (“ Specielle Pathologie u. Therapie ”) doubts the existence of asthma dyspepticum, and Riegel also (“ Die Erkrankungen des Magens,” Wien, 1896, S. 192). The literature on this subject is very limited, and many of the cases reported do not impress us as strictly belonging to the clinical picture of asthma dyspepticum. O. Rosenbach (“ Deutsche medizin. Wochenschr.,” 1879, No. 42) describes a number of cases 382 INFLUENCE OF GASTRIC DISEASES UPON OTHER ORGANS. which, although he separates them from dyspeptic asthma, very much resemble this clinical picture. The patient complained of oppression, want of air, difficulty in breathing, and a sensation of fear. The scarcity of reports on this complication is explained by the fact that the physician very rarely has an opportunity for ob- serving these cases during the attack ; as a rule, they cease spon- taneously within a few hours, and are frequently interrupted by the patients by mechanical manipulations to facilitate vomiting. It is well known that conditions of more or less anxious oppres- sion in breathing are observed occasionally in normal individuals, but more frequently in those afflicted with gastro-intestinal dis- eases. The attacks occur in connection with the larger meals, the patients having a feeling as if they could not breathe properly. The respiratory oppression and distress cease spontaneously during the course of digestion, or are relieved by eructation of gases. If these abnormal sensations are augmented, and when they occur at short intervals and after moderate ingestion of food, the condi- tion becomes pathological. A fear of smothering, with cyanosis, cool extremities, greatly hurried pulse, and dyspnea, occurring in the sequence of gastro-intestinal disturbances, represent a clinical picture which we are justified in designating as asthma dyspepticum. Oppler (“ Allg. med. Centralztg.,” 1896, No. 71) and Lauterbach (“ Wien. med. Presse,” 1894, No. 48) have each described one case of asthma dyspepticum as a sequence to gastric atony. The case of Oppler recovered under lavage, diet, massage, electricity, and the use of strychnin and belladonna. The cardinal symptom of the phenomenon is the paroxysmal dyspnea. It occurs most fre- quently among women, and especially among the neurasthenic and hysterical. Potain (Association pour PAvancement des Sciences, Montpellier, 1879) and Barie (“Revue de Medecine,” 1883, tome in, p. 1) have together reported thirty-two cases in France, a number of which gave indications that they were genuine asthma dyspepticum. Boas (“ Archiv f. Verdauungskrankheiten,” Bd. 11, S. 444) gives a very interesting report of eleven cases — ten males and one female. Instead of going into details concerning the symptomatology, we will describe a case which has been observed by the author repeatedly during attacks : The lady in question lived in the immediate neighborhood of the writer. Mrs. S., aged twenty-six, has suffered for years with symptoms of atony. Mother living and healthy ; father died with cancer of the stomach. She has DYSPEPTIC ASTHMA. 3«3 been married four years, but has no children ; heart and lungs normal. The dyspeptic symptoms are those of atony and nervous dyspepsia with hyper- acidity. There are no signs of enteroptosis ; right kidney is firmly attached in its normal position ; no history of uterine trouble ; constipation. Results of analysis of test-meal: Total acidity, 90; free HC 1 , 50; combined HC 1 , 22; ery- throdextrin present in excess ; lactic acid absent. Examination of the urine for toxic products gave the following results when it was first examined ; this was shortly after an attack, and was also followed by an attack on the next day: Preformed sulphates, 3.970 gm.; combined sulphates, 0.35 gm., — ratio, II. I ; urea, 51.028 gm. ; indigo blue, very strong reaction. December 14, 1896. — On this date the patient was very melancholy, and suffered much from intes- tinal flatulence. The writer was called just as an attack was beginning, and found the patient on the sofa, with the servants rubbing her hands and feet, which had a bluish tint and were quite cold to the touch. She had thrown open the windows on a cold night to get air, and was gasping for breath ; the pulse was 148. The patient was in mortal fear of smothering. There were marked cardiac oppression and a very peculiar wheezing sound with each breath, and tenderness to pressure in the epigastric region ; accentuation of the second cardiac sound. A stomach-tube was passed, and about 500 gm. of highly acid liquid drawn off, composed mostly of melted ice-cream and straw- berries. An enema was given containing warm claret and camphor, and hot bottjes were placed to the feet. The patient broke out in a perspiration within thirty minutes after the enema, and had quite recovered two hours after the attack. This same patient has since that time, which was a year ago, been seen in two other attacks very similar to this one, both of them yielding to the same treatment. Formerly, she had one attack every month, not in any con- nection with the menstrual period, however. Addition at time of revision, September, 1899. — With strict observance of diet and the use of alkalies this patient has not had an attack during the last fourteen months. There are no satisfactory explanations of asthma dyspepticum up to the present date. Potain ( loc . cit.) believes in a reflex irrita- tion from the gastro-intestinal tract, which causes contraction of the small pulmonary vessels. In the resistance to the pulmonary circulation which is thus brought about the respiratory gaseous exchanges are interfered with, and Potain, as well as Barie, claim to have found dilatation of the right ventricle, with accentuation of the second pulmonary sound during the attack. A. Frankel (article on “ Asthma ” in Eulenburg’s “ Real-Encyclopadie,” 3. Aufl.) considers asthma dyspepticum a reflex disturbance of car- diac asthma, caused especially by a weakness of the left ventricle, which then secondarily causes a passive congestion in the pul- monary circulation. This explanation concedes the trouble to be essentially cardiac asthma. There is a very intimate connection between disturbed digestion and cardiac action, which we have already dwelt upon, and the conception of Frankel is not without 384 INFLUENCE OF GASTRIC DISEASES UPON OTHER ORGANS. foundation in those cases in which the heart’s action is not per- fectly sound. Boas has reported cases in which the attacks were brought on by a disturbed gastric digestion, with bronchitis and emphysema. Abnormal gastro-intestinal meteorism may force up the dia- phragm mechanically, and if there is any debility about the pul- monary capillaries, passive congestion can not fail to occur. With the evacuation or escape of the gas the attack will cease entirely. Senator (“ Berlin, klin. Wochenschr.,” 1883, No. 22), G. Lewin, and Albu (Joe. cit.) claim that dyspeptic asthma is caused by the absorp- tion of toxic substances from the digestive tract. The theory of auto-intoxication has been criticized by Boas, since asthma dys- pepticum is not met with in any gastro-intestinal diseases associated with extensive putrefaction and fermentation ; whereas in those slight forms of gastric disease in which this asthma really does occur, there is very little formation of toxic products. Prognosis is favorable. Boas, Lauterbach, and Oppler have reported cures. One of the author’s cases has not had an attack for two and a half years following treatment. Treatment is mainly a prophylactic and dietetic one. The stom- ach should be sparingly treated, the bowels kept open, and all food causing flatulence must be scrupulously avoided. The underlying neurasthenia and pulmonary or heart affections should receive thera- peutic attention. In atony with hyperacidity, strychnin sulphate, of a grain, with extract of belladonna, -^-of a grain three times daily, and electricity can be recommended. During the attack itself speedy evacuation of the stomach by the tube and of the bowel by warm-water irrigation are the most effective means of treatment. The patients will usually not object to the tube in these attacks, because their suffering and want of air is so great that they are willing to undergo anything to be relieved ; but when it can not be used on account of heart or lung trouble, emetics should not be used either, because they are more depressing upon the heart than the use of the tube. When the heart is sound and emesis is absolutely indicated, we recommend the following : R . Pulvis ipecac., 1.5 gr. xxiij Antimon. et potass, tartrate, . . 0.05 gr. f. M. SlG. — Make two powders, to be taken one-half hour apart. Prompt emesis may be effected by the use of apomorphin, hypodermically, in doses of TTT of a grain ; but in most cases INFLUENCE OF NERVOUS DISEASES UPON THE STOMACH. 385 the vomiting unfortunately continues for some time after the stomach is evacuated ; it is, therefore, not recommended for this purpose. The Influence of Nervous Diseases Upon the Stomach. — This subject will be considered in connection with the various nervous disorders of digestion. It is a well-known fact that emotional excitement may cause an alteration in the gastric secre- tions, and that intense nervous depression may produce gastric distress, fullness, pressure, eructation, nausea, constipation or diarrhea, meteorism, and tenesmus. Mental overexertion may lead to nervous dyspepsia. Anatomical alterations in the central nervous system may be accompanied by motor, secretory, and resorptive disturbances. In this connection we refer again to the gastric disturbances occurring with tabes, and to the fact that Koch and Ewald caused gastric hemorrhages by cutting the spinal cord (“ Klinik d. Verdauungskrankheiten,” loc. cit.). Brown-Sequard and Schiff, as well as Ebstein (“ Archiv f. exper. Pathol.,” Bd. n, S. 183), produced gastric hemorrhage after experimental injuries to the anterior corpora quadrigemina. We have personally observed submucous hemorrhages and small areas of necrosis in the stomach eight days after section of one or both vagi in cats, dogs, rabbits, and guinea-pigs.* Malaria. — It is a very well-known fact, and generally accepted by the physicians of the Southern and Eastern States, that malaria very often complicates gastric diseases, and may even be an under- lying cause. It is very probable that a malarial state of the blood may be instrumental in causing gastric ulcer, which in this case has been asserted by London to be due to pigment emboli. In a case of pernicious malarial fever that died at Bay View Hospital there was found an abundant deposit of pigment between the pep- tic. ducts, and also within and between the cells of the ducts. At our clinic it is a standing rule to examine all persistent cases of stomach trouble for the presence of the malarial parasite in the blood. For the characteristics of this organism, and the methods of examination, we refer to the article by W. H. Welch and William S. Thayer, in the “ Loomis-Thompson System of Medicine,” and also to the able monographs of W. S. Thayer on this subject (“ Lectures on the Malarial Fevers,” London, Kimpton, 1898), also * If both vagi are intersected, the right one must be reached beneath the origin of the recurrent laryngeal nerve to preserve the sensibility of the respiratory passages. 386 INFLUENCE OF ANEMIA AND CHLOROSIS ON THE STOMACH. Thayer and Hewetson (“ The Malarial Fevers of Baltimore,” Johns Hopkins Press, 1895). In counties of the eastern shore of Vir- ginia malarial gastralgia is frequent. Malaria does not, as a rule, affect the secretion or motility, except in the various forms of per- nicious malarial fever.* In gastric troubles showing any period- icity, or microscopic or clinical evidence of malaria, quinin should be promptly administered, and if not effective within twelve hours, the hydrobromate of quinin should be injected hypodermically. Dr. Hans Herz, in his recent work (“ Disturbances of Digestion as a Cause and Consequence of other Diseases ”), does not mention malaria as a cause of disease of the stomach. Anemia and Chlorosis. — The relation between pernicious ane- mia and atrophy of the stomach has been considered, and the claim of Austin Flint to the priority of this clinical association has been emphasized in the chapter on Achylia Gastrica. Anemia and chloro- sis are influential etiological factors in the causation of gastric dis- eases, if they are primary conditions. This relation of the two states is very difficult to establish and probably very rare. Hayem (“ Des Alterations du chimisme Stomacal dans la Chlorose,” “ Bulletin Med.,” 1891, No. 87) asserts that the alterations in the stomach and intestines are the primary cause. Ewald and Rosenheim maintain that the digestive disturbances may be the results and not causes of the anemia. There are, undoubtedly, cases in which the anemia is the cause, and others in which it is the result. In some in- stances the treatment will throw light on this causative relation. If the secretory and motor functions of the stomach become normal with the cure of undoubted anemia, the gastric disturbance was the result of the state of the blood; but if the secretory and motor dis- turbances are marked, and perhaps of long standing, and examina- tions show only a slight deviation from the normal state of the blood, the digestive disturbance is the primary one. Often it is possible, when patients remain under observation for a long time, to observe the progressive anemia developing as a sequence to gastro-intestinal atrophy. The effect of syphilis on gastric digestion has been considered in a separate chapter. * A very reliable and accurate Southern colleague informed us of a case of periodical hematemesis, which he had observed near Savannah, occurring every third day, which was cured by quinin. A form of the algid, pernicious malarial fever is called by some Southern doctors “gastric malarial fever.” EFFECT OF PULMONARY DISEASES ON THE STOMACH. 387 Respiratory Organs — Mouth, Nose, Pharynx, and Larynx. — Numerous inflammations of these parts may cause invasion of the stomach, by direct infection — i. e., swallowing of infectious material. Abnormalities in the formation of the gums, cleft palate, deviations of the septum, retracted gums, or chronically enlarged tonsils may, by causing one of the many forms of stomatitis, or, compelling mouth-breathing, bring on gastric disturbance. Stenoses of the nasal passages in gastric sufferers imperatively demand correction ; in short, all conditions leading to mouth-breathing may induce dyspepsia. If this is the case with simple catarrhal changes, it is of course much more serious with carcinoma, syphilis, tuberculosis, or other destructive processes (noma) about the mouth, nose, throat, larynx, and antrum of Highmore. In persistent gastric hyperacidities we have frequently observed what may be termed a reflex pharyngitis and posterior nasal catarrh, which were permanently cured by treatment of the hyper- acidity after direct throat and nose treatment had failed. The amount of mucus in the pharynx became largest when the gastric acidity was highest; at this period the hawking and spitting were incessant ; they became less as the acidity was reduced either by normal evacuation of the stomach or the use of alkalies. The latter were in some cases poured in through the stomach-tube, when their beneficial action on the pharyngeal mucous flow was also very evident. Pulmonary Diseases. — The most prominent among these is pulmonary tuberculosis. W. Fenwick found gastritis to be present in nearly all the cases of pulmonary tuberculosis, chronic bron- chitis, emphysema, and acute pneumonia. He asserts that in dis- eases of the brain no gastric involvement was observed by him (“Virchow’s Archiv,” 1889, Bd. cxviii, S. 187); he found gastritis in eleven cases out of fifteen of phthisis. Marfan (“ Troubles et Lesions Gastriques dans la Phthisie Pulmonaire,” Paris, 1887) found but five cases in sixty-one of tuberculosis in which the gas- tric symptoms preceded the pulmonary. It is very difficult to decide, when a dyspeptic is at the same time affected with pul- monary tuberculosis, which trouble is primary. As a rule, dis- eases limited to the stomach can not so weaken the general state of health as to predispose to pulmonary tuberculosis. Rapid exhaustion from localized gastric diseases occurs only in carci- noma, which is in itself rapidly fatal before lung trouble is devel- oped to any great extent; but when the gastric disease is associated 388 INFLUENCE OF OTHER DISEASES ON THE STOMACH. with intestinal disturbances, so that the digestion is very much interfered with, general nutrition may be so impoverished that tuberculosis can be more readily acquired. Hutchinson (“The Morbid States of the Stomach and Duodenum,” London, 1878) publishes an analysis of a large number of cases, and states that the digestive disturbances precede the tubercular infection in about one-third of the cases. It is in these cases of suspected pulmonary disease, associated with digestive troubles, that the ability of a good auscultator will tell. Gastro-enterologists should not fail to avail themselves of their experience in auscultation and percussion. Whenever sputum can be obtained, it should be examined for tubercle bacilli. The state of the gastric secretion and the motor function in tuberculosis have been studied by Edinger ( loc . cit .), Rosenthal {loc. cit. ), Shetty (loc. cit.), O. Brieger (loc. cit.), Immer- mann (loc. cit.), Hildebrandt (loc. cit.), and Einhorn (loc. cit). The state of the secretory and motor functions in pulmonary phthisis varies, in our experience, with the stage of the pulmonary disease. In the incipient stages of phthisis, secretion and motility may be normal for a long time ; they will become more and more deranged as the pulmonary trouble progresses, so that in the final stages of pulmonary caseation, breakdown, and formation of cavities, all gas- tric function may be extinguished. Brieger (loc. cit.) states that in the initial stages the cases of normal and disturbed secretion are about equally divided. In moderately severe cases secretion was normal only in one-third, or 33 per cent. ; in the remainder secre- tion was variable, but generally depressed. In 6.6 per cent, there was no secretion whatever. In advanced cases of phthisis secre- tion was normal only in 16 per cent, of the cases. It was more or less defective in the rest of the cases, and in 9.6 per cent, there was complete arrest of secretion^ Immermann (loc. cit) found the gastric peristalsis normal in fifty-three put of fifty-four tests, whereas Klemperer (loc. cit.) claims to have found marked inhibi- tion of the peristalsis by his method. The amount of gastric secretion and the state of the peristalsis are not satisfactory expon- ents of the digestive powers of phthisical patients. The only correct way to find out whether such patients have digestive power sufficient to maintain the nitrogen equilibrium is by quantitative experiments on metabolism. By giving weighed amounts of certain foods after the nitrogen balance has been established, and deter- mining the quantity that is digested and the quantity that is excreted undigested, together with careful determination of the EFFECT OF PULMONARY DISEASES ON THE STOMACH. 389 amount of nitrogen in the urine, we have been able to discover that tuberculous patients (first stage of pulmonary tuberculosis), with absolute achylia gastrica, may, with care as to diet, still be able to maintain their nitrogen equilibrium, provided the gastric peristalsis was preserved. In future the exact state of the pulmonary disease, its duration and extent, together with a statement of the condition of all the remaining organs, would be desirable, if the correlation existing between gastric and pul- monary troubles is to be put upon a basis of approximate exactness. Although the treatment of the tuberculosis is the main object, it will be impossible to maintain nitrogen equilibrium with a defective digestive apparatus ; it is, therefore, essential that the functions of the stomach should be improved as far as possible. In this way a system of forced alimentation, such as has been very successfully employed by Debove (loc. cit.), Dettweiler, Lieber- meister, Leyden, Riihle, and Peiper, may become possible. In each individual case the diet and the medicine should be ordered according to the state of the gastric functions found from test- meals. We have had three patients affected with pulmonary tuber- culosis and gastritis at the Maryland General Hospital during the winter of 1896 and 1897, who gained considerably in weight by treatment of the existing gastritis. One patient with pulmonary tuberculosis and a tubercular rectal fistula gained fourteen pounds in two months under daily lavage and administration of HC 1 and strychnin, together with nutritious diet. * Diseases of the Heart. — We have already spoken of the effect of gastric disturbances in producing tachycardia, bradycardia, and arrhythmia. The diseases of the stomach which are caused by valvular affections of the heart are brought about by the venous stasis and passive congestion. Under the head of chronic gastritis we have spoken of the efficacy of digitalis when valvular disease is in clear etiological association with the gastric affection. Concerning the state of the secretion in heart diseases, there is no agreement in the observations thus far reported. In twenty patients with heart disease Adler and Stern (“ Berl. klin. Wochenschr.,” 1889, No. 49) found free HC 1 always present in sixteen, variable in two, and always absent in two cases. Huff er states that in ten cases of mostly valvular lesions suppression of the secretion of HC 1 and absence of *The tuberculous fistula was treated by Dr. Samuel T. Earle, and healed up com- pletely before the patient left the hospital. i 390 INFLUENCE OF OTHER DISEASES ON THE STOMACH. albumin digestion were found nine times and hyperacidity in a single case. Most of his patients are stated to have been in the stage of perfect cardiac compensation. These observations of Hufler are not intelligible in the light of the pathological physiology of cardiac diseases ; for perfect compensation means that the arterial and venous pressure in all the organs is normal ; under this state we can not conceive of any passive congestion in the stomach. Ger- main See held that the initial “ Gastricismus ” was the earliest sign of a valvular trouble ; that evidence of passive congestion may be present when there is as yet no murmur or accentuated sound. By perfect compensation we mean the natural compensation of the heart-muscle, not the transient improved tonus effected by a drug (digitalis). In our experience gastric secretion was normal in eight cases of mitral regurgitation, two cases of aortic regurgita- tion, and two cases of mitral insufficiency, with perfect compensa- tion. As soon as compensation becomes defective, the gastric symptoms make their appearance, and secretion is found altered. Diseases of the Liver. — The close anatomical and physio- logical relationship between the liver and the stomach explains the sympathetic manner in which diseases of one organ fre- quently reflect upon the other. Excepting in the diseases of the biliary passages and gall-bladder, it is impossible to say which organ is primarily affected. During the passage of gall-stones gastric secretion is suppressed ; this suppression is due to a reflex influence caused by the intense pain. We have analyzed the vomited matter which was brought up during attacks of biliary colic: In three cases it was neutral, very faintly acid (= 6°, decinormal NaOH) ; in one case it showed presence of combined HCl — no free HC 1 ; in two cases it was alkaline (= 8°-io°, H 2 S 0 4 ). The alkalinity of this vomit was not due to the presence of bile or pancreatic juice, because they were found to be absent. Cases of cirrhosis of the liver, and even of cancer of the liver, may run a latent course for a long time, the symp- toms being those of chronic gastritis. We have made 1 1 8 analyses of gastric contents in cases of catarrhal jaundice (“ Bulletin of the Maryland University Hospital,” vol. in, No. 2, p. 30). In twenty cases of icterus (catarrhal) free and combined HCl were absent in twelve ; free HCl absent but combined HCl present in four; free and combined HCl present in six. It would, of course, be important to know whether those cases in which free HCl was absent during the icterus had chronic gastritis before the jaundice. EFFECTS OF DIABETES AND RENAL DISEASES. 39 1 In six of these eight cases free HC 1 was found two months after the recovery from the attack at that time there were no evidences of gastritis. Gout and Rheumatism. — Burney Yeo claims that dyspepsia is a frequent and prominent manifestation of gout(“ Brit. Med. Jour./' Jan. 7 and 14, 1888). This specific gouty disorder of the stomach is claimed to exist in states of uric acid diathesis by a number of contributors to British medical journals. Ewald states that he has not met with a single case of true gout with coincident gastric dis- turbances, but that he has seen numerous such examples in chronic articular rheumatism, in which the dyspepsia was so marked that the pains in the joints were comparatively insignificant. Anomalies of secretion in gout have been repeatedly observed by us. The most frequent secretory trouble is hyperacidity. Alexander Haig recognizes gout of the intestines and cecum (“Uric Acid as Causation in Disease,” pp. 330 and 623), also gastro-intestinal irritation, as a cause of uricacidemia (loc. cit., p. 49). Without entering into the literature of the relation of uric acid, gout, and rheumatism to gastro-intestinal diseases, we wish to say that the nature of these diseases is still too obscure to permit of any exact scientific determinations of the relation in question. Gout and uric acid diathesis occur in the same constitutions, sug- gesting that the conditions are identical. The author has had occasion to study numerous cases of gastralgia that yielded to nothing but salicylate of soda and colchicum, also many cases of enteritis that were improved by diet free from uric acid (milk); still, these observations do not convince him of the correctness of the terms “ gout of the stomach or intestines ” which Haig uses. Diabetes Mellitus. — Although there is no constancy in the character of the secondary gastric symptoms accompanying diabetes, there are few cases of this disease in which the stomach is not involved. Diabetes affects the stomach in two ways prin- cipally : either by arresting its functions through auto-intoxication or by production of gastritis. The presence of great thirst, polyuria, polyphagia, ocular disturbances, pruritus, emaciation, usually means coexistent gastric involvement. Rosenstein and Gans have examined the gastric functions in diabetes (Rosenstein, “ Berl. klin. Wochenschr.,” 1890, No. 13). Their results show that the disturbances, although present, show no constancy in type. The polyphagia and polydipsia of diabetes have been known to cause gastrectasia. Our personal observation on diabetic patients 392 INFLUENCE OF OTHER DISEASES ON THE STOMACH. indicates that, as a rule, peristalsis and secretion are normal. Our material in this line has been limited. Eight normal tests of both functions were found in twelve cases studied. In the abnormal cases, hyper-, sub-, and anacidity were found in different patients, and in the same patient at different times (heterochylia). There is no sugar present in the gastric secretion (Kiilz). The disease has been known to begin with severe gastric symptoms from the onset, and Teschemacher advises that the urine be examined for sugar in all cases where severe acute gastritis repeatedly occurs without a traceable cause. Diseases of the Kidney. — The stomach is always more or less affected in renal diseases, and the symptoms of disturbed gastric digestion very often appear long before albumin is present in the urine. In the “ Maryland Medical Journal,” July 24 and 31, and August 7, 1897, I have reported three cases of nephritis which were probably due to chronic auto-intoxication from the gastro- intestinal tract. In this connection I wish to emphasize the gastric diseases which are caused by preexisting affections of the kidneys. Naturally, it is unavoidable that a certain amount of auto-intoxication will accompany the association of renal with gas- tric disease, no matter which is the primary affection. Albu (Joe. cit . ) and Biernacki (“ Berk klin. Wochenschr.,” 1891, No. 25 and No. 26) emphasize the influence of retained metabolic products in producing gastric disturbances. These retained products of metab- olism injure the stomach in two ways : (1) By acting as toxins through the vascular channels directly upon the parenchyma of the gastric walls, and (2) by irritation of the surface of the stomach, since they are very frequently excreted in this manner. Fenwick (loc. cit) states that the gastric mucosa is capable of secreting urea like the intestinal mucosa, and that the excretion of this product causes an acute catarrh of the gastric glands. I have analyzed the vomit of two patients afflicted with chronic interstitial nephritis, and repeatedly found urea or ammonia in it. If the total nitrogen excreted in the urine is approximately normal, the vomit does not contain urea, in my experience. This would indicate that the gastro-intestinal canal is not called upon to vicariously secrete urea, until the kidneys can no longer do so. A variety of gastric diseases have been found to exist in connection with chronic Bright’s disease. We shall see in the clinical part that acute and chronic gastritis, fatty degeneration of the glandular epithelium, and, according to Ewald, amyloid degeneration may occur. Edema of RELATION OF RENAL AND GASTRIC DISEASES. 393 the gastric walls is a very rare complication. The effects of floating kidney in producing stenosis of the duodenum have been con- sidered in the chapter on Enteroptosis. Allan A. Jones (“ Gastric Conditions in Renal Disease,” “ New York Med. Jour.,” Jan. 19, 1895) has frequently found suppression of gastric secretion in patients with kidney diseases. Einhorn reports a case of achylia gastrica due to renal calculus, which had existed for a long time. After removal of the stone by operation, the gastric symptoms at once disappeared. According to Biernacki, the secretory function is arrested in renal affections. Renal Disturbances in Connection with Digestive Diseases. — During disturbed digestion a number of toxic substances formed in the gastro-intestinal canal reach the kidneys through vascular channels, and are there excreted. Substances very closely related to serum-albumin find their way out through the kidneys : for in- stance, albumoses, egg-albumen, and hemoglobin. Under this increased work the kidneys may become diseased. In experi- mental injections of egg-albumen it has been observed that more albumen is excreted than was injected. If the disturbance persists for a long time, albuminuria, excretion of epithelia', and leukocytes become more permanent. There are abnormal conditions of the blood in which the excre- tion of the urine may become totally suppressed : for instance, the blood disintegration after grave icterus and extensive burns. There are two kinds of renal albuminuria: (1) Those due to pathological changes in the parenchyma or innervation or vascular supply of the kidney, and (2) the hematogenous variety, in which a primarily healthy kidney serves as a purifying organ to excrete useless albuminous substances. Both varieties may occur com- bined, for the same cause may alter blood and kidney simultaneously (scarlatina, typhoid fever), an), miliary abscesses, between which they are but little less numerous. The fibers of the muscularis mucosae have been widely separated by these cells. Few cancer cells are to be seen in this portion of the tissue, but in one place (C) they afe found plug- ging completely a small vessel. In the upper part of the submucosa a few of the cancer cells can also be seen (Z>). PATHOLOGY OF PHLEGMONOUS GASTRITIS. 435 time.* Most authors who have had experience with the disease distinguish, first, an idiopathic primary purulent gastritis, the eti- ology of which is obscure; and, secondly, a secondary, metastatic, phlegmonous, or purulent gastritis, which is an accompaniment or a sequence of other infections, such as pyemia, puerperal fever, anthrax, typhus, or variola. Anatomically, one may distinguish a diffuse and a circumscribed purulent inflammation of the submu- cosa ; the latter is spoken of as a stomach abscess. Etiology. — The direct cause of the rarer idiopathic phlegmon- ous 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 bac- terial invasions of the submucosa, principally by pyogenic cocci that find portals of entry through lesions in the superficial epithe- lium of the stomach, such as occur in most gastric diseases, espe- cially in so-called exfoliation in carcinomata and old ulcers, or after trauma caused by fish-bones, seeds, foreign bodies, etc. Ziegler’s bac- teriological ( loc . cit.) studies have already been mentioned. The sec- ondary metastatic phlegmonous gastritis, which seems most fre- quent, is that following puerperal fever, and owes its origin to locali- zation in the stomach of the specific organisms producing the funda- mental disease. Whatever they may be, it is self-evident that only an enfeebled organ is liable to such an inflammation, since pyogenic cocci can not resist the action of the free HC1 of the gastric juice. Pathological Anatomy. — The diffuse inflammation rarely in- vades all parts of the stomach with the same intensity, even if the whole organ is involved. The pyloric portion is generally invaded more than the others ; toward the cardia the inflammatory process is less and less marked, while the esophagus is rarely attacked. The submucous layer is most extensively altered ; on cross-section it is swollen, showing an edematous, purulent, or, at times, a bloody infiltration. From here the inflammation spreads along the inter- glandular 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 by accumulations of pus. Rokitansky has described a case in which the mucosa was only strikingly anemic * We have collected the entire literature on the subject of phlegmonous gastritis, which is appended. 436 PHLEGMONOUS GASTRITIS. otherwise unaltered. Macleod (“ Lancet,” 1887, vol. 11, p. 1166) de- scribes a gastric abscess in which mucosa was said to be unaltered. 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 per- foration, as a rule, rapidly follows inflammation of this layer. Circumscribed abscesses, which must be differentiated from the diffuse inflammation, are usually small, varying from the size of a hazelnut to that of a goose egg (Leube, loc. cit.). On cutting into the swollen elevated areas of mucous membrane, the abscess is found in the submucosa, but may extend through the muscularis to the serosa. Symptomatology. — The symptoms are very much like those of a very intense simple acute gastritis ; the pain of gastric phlegmon is not materially increased by change of position or pressure. There is very rarely any vomiting of pus in diffuse purulent gas- tritis. 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 disappear 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 some- times break through into the stomach and cause the same symp- toms. The fever reaches I04°-I05° F., the patient being aware from the outset that he is very seriously ill. The sensorium is much disturbed by great restlessness, headache, insomnia, delirium. To the symptoms of acute gastritis those of a sudden peritonitis may be added at any time. Diagnosis. — The important conditions for diagnosis are the pain, vomiting, meteorism, fever, diarrheas, and general phenomena. The pain is localized in the epigastrium, but is said to have been absent in some cases. The emesis is always present, and consists of bile, mucus, and food debris; in diffuse purulent gastritis, pus has not been noticed in the vomit, which strongly resembles so- called peritoneal vomiting. The fever is very high, and the temperature curve is said to resemble those of pyemic fevers, with marked remissions and ex- acerbations. Tympanites and diarrhea are more frequent than con- stipation. Other symptoms are : rapid, compressible pulse, cold peripheral parts, hurried respiration, thirst, and a much- coated PHLEGMONOUS GASTRITIS. 437 tongue. The course of gastric abscess is not characteristic, and Leube states (“ Spec. Diagnose d. inneren Krankheiten,” S. 237) that the diagnosis is a matter of chance. The attack may resemble a circumscribed peritonitis or one of the various perigastric inflam- mations or abscesses ; according to Ewald ( loc . cit.) it may so mimic abscess of the spleen or left lobe of the liver that a differential diagnosis is absolutely impossible. Deininger(“ Deutsches Archiv f. klin. Med.,” Bd. xxm, 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 char- acteristic to justify a diagnosis. These symptoms, however, occur also in above conditions referred to by Ewald. Chvostek (“ Wiener Klinik,” 1881, and “ Wiener med. Presse,” 1877, Nos. 22-29), how- ever, seems to have made the diagnosis in one of his cases. The case reported by the author (“ A Case of Phlegmonous Gastritis,” etc., by Hemmeter and Ames, “ New York Medical Record,” loc. cit.) was not diagnosed antemortem. The condition of diffuse suppurative gastric inflammation had followed an ulcus carcinoma- tosum, which had been recognized and successfully treated as a simple ulcer by my associate, Dr. E. L. Whitney, fourteen months before death occurred. When there is probability of diffuse or cir- cumscribed phlegmonous gastritis, the exploratory puncture with an aspirating needle, or the exploratory incision, is, in our opinion, justifiable. In Penzoldt and Stintzing’s new “ Specielle Therapie innerer Krankheiten,” volume iv, page 446, von Heinecke gives suggestions for the operative treatment of phlegmonous gastritis. Prognosis is almost always unfavorable, especially in the diffuse form. After the circumscribed form and evacuation of the abscess, several clinicians have reported recoveries (Deininger, loc. cit., Glax, loc. cit., Kirchmann, loc. cit., also Buckler, “ Idiopathic Phlegmon. Gastritis,” “ Bayerisch. Aerztliches Intelligenzblatt,” 1880, No. 37), but it is impossible to confirm whether they were really gastric abscesses. Dittrich has found cicatrices in the submucosa pointing to the possibility 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 treat- ment can be only symptomatic and limited to relieving pain by hypodermic injections of morphin, applications of ice, — ice-bag to the stomach, crushed ice by the mouth. To counteract collapse, wine enemata and hypodermic injections of strychnin may be rec- ommended. Medicines by the mouth are worse than useless. 43 » INFECTIOUS GASTRITIS. INFECTIOUS GASTRITIS. (i Gastritis infeciiosa , diphtheritica , crouposa, mycotica , parasiiaria.) As Penzoldt correctly remarks (/0c. cit.), every gastritis is to a certain extent infectious ; for this reason a number of authors reject the conception of infectious gastritis as a separate and distinct dis- ease. Lebert ( loc . cit.) and Oser (article on Gastric Diseases in “ Eulenburg’s Realencyclopadie,” second edition, volume xii, p. 410) believe that there is a characteristic infectious gastritis peculiar to itself. Boas (“ Spec. Therapie d. Magenkrankh.,” p. 6) is of the opinion that there is a form of acute gastroenteritis, well character- ized 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 consid- eration to infectious gastritis. Those that establish a separate category for this affection class under this head all gastric inva- sions 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 protracted, as it may last, according to Boas, three to ten days. According to Lebert (loc. citl), some cases may have fever for two to three weeks. In this case the Widal method (loc. citl) should be made use of under such conditions to distinguish them from enteric fever. Gaffky (“ Deutsch. Med. Wochenschr.,” 1892, No. 14) gives an account of severe gastroenteritis in three persons who drank the unboiled milk of a cow affected with hemorrhagic enteritis. He believes that the infecting germ was a particularly virulent type of the bacillus coli communis. A num- ber of similar mass epidemics are on record (Husemann, “ Deutsch. med. Wochenschr.,” 1889, S. 960) that tend to strengthen the conception of a special infectious gastritis. There seems no neces- sity as yet for a separate classification of this kind; the subject is still too hypothetical to be ranked as equal in importance with other well-characterized forms of gastritis. The diagnosis, prog- nosis, and treatment are said by Boas to be the same as for acute simple gastritis. Diphtheric gastritis is a rare affection, occurring not only as PLATE VI. Bacterial Invasion of Gastric Epithelium. From a Case of Diphtheric Gastritis. — ( Hemmeter . ) 29 MYCOTIC GASTRITIS. 439 a sequence to laryngeal and pharyngeal diphtheria, but also as an accompaniment to pyemia, septicemia, puerperal fever, scarlatina, variola, endocarditis, ulcerosa, typhus, etc. The disease is, as a rule, not discovered until the autopsy is made, and for that reason has more of a pathological than clinical interest. Mycotic Gastritis* — When the vitality of the mucosa and the secretion of hydrochloric acid have been reduced, suppressed, or destroyed, certain pathogenic 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. Among those that have been described are the anthrax gastritis, produced by spores or bacilli of anthrax lodging in the mucosa or submucosa, and giving rise to inflamma- tion, ulceration, 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 cheek, where a malignant pustule developed (“ Journal of Pathology and Bacteriology,” vol. i). Gastritis caused by the favus fungus (achorion Schonleinii) has been reported by Kundrat (“ Ueber Gastro-enteritis Favosa,” “ Wien. med. Blatter,” 1884, No. 49). The case was that of a drunkard whose gastric mucosa was predisposed by alcoholic chronic gas- tritis; he had favus universalis, and in the stomach and intestines the fungi had caused diphtheric inflammations, with fibrous exuda- tions, ulceration, and sloughing ; death was caused, it appears, by a terminal colitis. The thrush fungus (German, Soor ; Latin, Oidium albicans') has been reported as setting up a mycotic gastritis ; in some cases the stomach alone appeared infected, throat and esophagus being intact. The yeast fungus (torulae or saccharomyces cerevisiae), sarcinae, the common molds (penicillium glaucum and mucor) 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 products of the fermentation which they cause. Sarcinae, according to Huhne, do not bring about any fermenta- tion. Miller’s interesting investigations concerning the bacterial flora of the mouth have been referred to on page 63. Orth, in the first volume of his excellent text-book (“ Specielle pathol. Anatomie,” Bd. 1, p. 704), describes an interesting bacterial invasion near an 440 PARASITIC GASTRITIS. old chronic gastric ulcer which had largely healed. At several places there were grayish, bran-like incrustations, partly adherent, which anatomically had to be designated as diphtheric. 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 supposition could not, however, be confirmed by cultures. The case was complicated by the fact that a fatal hemorrhage had occurred from a very small arteriole at a place where only a very tiny defect in the mucosa was observable. In the immediate neigh- borhood of this defect the bacilli were found also, but not in suffi- cient numbers to attribute to their destructive agency the tearing of the arteriole, which was not aneurysmatic. Orth then refers to the bacillus gastricus, or polysporus brevis of Klebs (“ Ueber Infectiose Magenaffectionen,” “Allgemein. Wien. med. Zeit.,” 1881, Nos. 29 and 30), which this pathologist claims to have 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 (“ Dorpater med. Zeitschr.,” 1875, p. 184) also de- fended the view that gastric ulcers are in part due to mycotic and bacterial invasions. Unfortunately, Klebs’ and Bottcher’s state- ments 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. in, S. 522) gave an account of acute gastritis set up by larvae (maggots) of diptera, a class of insects of which the common fly, the flea, etc., are examples. The eggs of these larvae were said to have been swallowed with raspberries. Meschede (“ Ein Fall von Erkrank. durch im Magen weilende lebende Maden,” “ Virchow’s Archiv,” Bd. xxxvi, S. 300) reports gastritis caused by maggots eaten with cheese. Senator reported gastritis set up by living maggots of the common fly, which occurred 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 observed a case of gas- tritis and gastralgia caused by an earthworm (“Journal de Med. Practique de Paris,” 1836, tome vn, p. 57). It is known also that ascarides and tape-worms may reach the stomach in rare cases and give rise to severe inflammations, which may subside at once as soon as the offending parasite is vomited. TOXIC GASTRITIS. 44 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 with suicidal intentions, are mercuric chlorid or corrosive sublimate, phosphorus, arsenic, chloroform, creasote, potassium chlorate, oxalic acid, nitrobenzol, carbolic acid, the concentrated inorganic acids, sulphuric, hydrochloric, and nitric acids; the caustic alkaline hydroxids in strong solution, and, furthermore, alcohol in all its forms, and some substances used as medicines (see etiology of acute gastritis), particularly croton oil, antimonium and potassium tartrate (tartar emetic) ; also ammonia. The pathology will necessarily vary considerably, as it is not only dependent upon the kind, but upon the quantity and con- centration of the poison ; and also upon the circumstance whether the poison is taken on a full or an empty stomach, as food and drink dilute the drugs. There may be only a slight superficial inflam- mation, or a very penetrating corrosive effect involving the entire gastric wall and even leading to perforation. Different drugs produce different effects upon the mucosa. Phosphorus, arsenic, antimony, and alcohol produce, in excessively large toxic doses, a milky, yellowish-white, or opaque appearance. The epithelia of the alveoli of the tubular glands are partly in a state of mucoid degen- eration, partly finely granulated, cloudy, and showing fatty degen- eration ; 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. y when the poisons are not taken sufficiently strong to effect ulceration or to destroy secretion. Dilute acids and alkalies induce the clinical picture of a simple acute gastritis ; while, in concentrated form the same agents cause a deeply penetrating necrosis, formation of crusts and intense reactive inflammation with serous infiltration, suppuration, and blood extravasation. The scabs or crusts show different colors with different corrosives. Under the effect of sulphuric acid they are black; of nitric acid, yellow ; of alkalies, brown ; of copper salts, green or blue ; of silver salts, black. Dislodgment of these crusts leads to fatal bleeding, tearing of the serosa, or perforation, with peritonitis. Oxalic acid is said to produce a jelly-like, semitrans- parent swelling. Ammonia causes a pustular inflammation. Symptoms . — After taking the poison there is generally an inde- scribably severe pain, intolerable burning, and vomiting which in- 442 TOXIC GASTRITIS. creases the pain and at times causes fainting. The vomit, as a rule, contains blood or bloody mucus. The thirst is great. There is most frequently diarrhea containing blood. Severe general symptoms follow : small, very fast pulse ; jactitation ; delirium. In case much of the poison has reached the general circulation, hematogenous icterus, petechiae, albuminuria, and hematuria may follow. Death may follow in a few hours or a 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 from hemorr- hage when the scabs and crusts are sequestrated, or by sequelae — i. e., stenosis of the esophagus, cardia, pylorus, or atrophy of the mucosa. The diagnosis , after learning 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 evident. The prognosis of severe toxic gastritis is necessarily grave ; if not from the direct poisoning or first destructive effect of the drug, certainly from the severe secondary effects. The treatment will vary with the nature of the poison. In recent poisoning with strong acids, magnesia usta (calcined) should be given as soon as possible. If no drug-store is near, chalk, or even powdered lime, which can be scraped from the wall, should be given. Whenever possible, the stomach-tube should be used at onceffor all poisoning of recent date. Boas, Fleischer, and Pick advise that the tube should not be used in severe acid or caustic alkali poisoning, because of the danger of perforating the stomach. In six cases of poisoning — one with lye (KOH), two with oil of vitriol (H 2 S 0 4 ), one with strong ammonia (NH 3 ), and two with carbolic acid — the tube was used immediately after the patients reached the hospital. As such cases run great danger of a corrosive perforation, we have personally used the tube and let the patient take his chances, which were better in these cases than in those where the tube was not used. About 250 c.c. of water, with sodium bicarbonate in case acids h'ave been taken, or vinegar in case of alkalies, is indicated to dilute and combine with the destructive agent present. Lemon juice will also answer for the alkaline 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. The approved antidotes should be given (freshly prepared hydrated oxide of iron for TREATMENT OF CHRONIC GASTRITIS. 445 arsenic, etc.), that will be found in various text-books on toxi- cology and therapeutics (H. A. Hare’s system; H. C. Wood; Lauder Brunton ; Binz, Schmiedeberg ; Penzoldt and Stintzing’s system, vol. iv). After carbolic acid ingestion, wash out the stomach, and then pour in 250 c.c. olive oil. In all corrosive poisoning cases the pouring in of olive oil or molten vaselin, after neutralization and washing out, will, if possible, diminish the corrosive effect. When not too much acid or alkali has been taken, the subnitrate of bismuth or subgallate of bismuth, one dram twice a day, swallowed with oil, will favor rapid cicatrization and inhibit bac- terial infection of the necrosed, charred areas. A suspension of bismuth subnitrate, three drams to one pint mucilage and water, has proved advantageous in a case of carbolic acid poisoning in our practice ; it was used in form of lavage. Another was healed of long standing gastric ulcerations by blowing in bismuth subnitrate and subgallate through a stomach-tube — dry, not in suspension. If the pain is severe, morphin must be promptly given, hypoder- mically, in to of a grain doses, repeated until relief comes. It is our duty to give relief of the pain at any risk, even if chloroform anesthesia is required ; for after the suffering ceases our efforts to save the patient can be more easily executed. Nutrition must be carried on by rectal enemata only. By the mouth, ice is about all that is permissible ; it will tend to diminish the pain, fever, and inflammation. We make so explicit a statement of treatment because we had experience with two cases where the autopsy showed that recovery might have been possible (as not much sul- phuric acid had reached the stomach) if the treatment had been more heroic — i. e., if the tube had been used for timely removal of the poison. CHAPTER II. CHRONIC GASTRITIS. Little over a decad ago it was customary to designate all stomach diseases that were not acute, and that could not be diag- nosed as dilatation, ulcer, or carcinoma, as “ chronic gastric catarrh.” We agree with Ewald and Penzoldt in the objections to the word “ catarrh,” and have given the reasons under the chapter on Simple Acute Gastritis. Even at the present day there is no 444 CHRONIC GASTRITIS. absolute uniformity in the conception and limitations of the term “ 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 so-called 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 the important functions, although one or the other of these is generally most involved. There are observed many varia- tions in kind and intensity of disturbed function, from a trivial reduction of secretion of gastric juice or interference with motility, to complete suppression of glandular activity and pronounced insufficiency of peristalsis. There are two pathological processes inseparable from every chronic gastritis ; these are : degeneration and desquamation of the glandular cells, and infiltration of con- nective tissue. Bearing in mind these conditions, we may distin- guish two main types of chronic gastritis: first, the hypertrophic; and, secondly, the atrophic. The hypertrophic form consists of proliferation of the connective tissue, leading to change of form and folding or warty elevations of the mucosa (“ etat mammelone,” or polyposis). The result of this process is, first, either complete destruction, or, secondly, cystic degeneration of the glands. A grayish-brown, or, in places, a dark brown, color is peculiar to this swollen and proliferated mucosa, which is covered with an adherent, gray coating of mucus. The atrophic form consists of contraction of the connective tissue, loss of 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 grayish- white or pale slate-gray color. If this process attacks the muscu- laris and submucosa, it may cause atrophy of the muscle fibrils, with or without thickening of the entire gastric wall due to new formation of connective tissue. Then, again, we may meet with a genuine hypertrophy of the muscularis, particularly at the pyloric portion, or in the pylorus itself (hyperplastic stenosis of the pylorus). The lumen of the stomach in these forms may show a normal capacity; or it may be much diminished in size by con- nective-tissue thickening of the gastric walls and subsequent con- traction. This process is known as “ gastric cirrhosis ” (Brinton). By French writers it is termed “hypertrophic sclerosis of the stomach ” (Hanot and Gombauldt, “ Archiv de Physiol.,” ix, p. 412 ; ETIOLOGY. 445 also Dubey, “ Gazette Hebdomin.” 1883, p. 198), and it may reduce the normal capacity to 160 c.c. (Leube, Penzoldt). Or, again, the capacity is much increased by a dilatation in consequence of chronic gastritis and hypertrophic pyloric stenosis. So the anatomical picture may present: {a) atrophy of the mucosa with wasting of the peptic glands and of the muscularis ; thinning of the entire gastric wall, and, very frequently, dilatation; or, on the other hand, ( b ) inflammatory hyperplasia of the layers of the stomach, with excessive connective-tissue proliferation (cirrhosis ventriculi) ; hypertrophic pyloric stenosis; atrophy of the glandular layer and sometimes of the muscularis.* This form may lead to marked reduction of the lumen if the hypertrophy invade all layers uniformly. But if it attack the pyloric portion only, there may be a dilatation. Both forms produce grave disturbances of motility, secretion, and absorption. 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 mucous layer grows much more rapidly than the submucous 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. 1, p. 709). A number of Germans describe a variety of special forms of chronic gastritis under the names of “ saurer Katarrh ” (sour, or acid, gastritis), “ Schleimkatarrh” (slimy, or mucous, gastritis), also termed “ gastritis atrophicans,” and a simple chronic gastritis, or “ einfacher Katarrh.” All of these terms are, unfortunately, chosen 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, the result of secondary irritation of the mucosa. Etiology. — Chronic gastritis is a wide-spread disease, occurring in all stations of life, but most frequently among the poorer classes, where the quality of the food may be so inferior as to keep the stom- ach in a state of constant irritation. All the numerous injurious influences which arise from a defective and inappropriate diet have been referred to under the head of the pathogenesis of acute gas- tritis. It may evolve from the acute or subacute form, where the mucosa has been damaged by the altered circulation and its resist- *See Hemmeter and Stokes, “Chronic Hypertrophic Gastritis,” etc., “Jubilee Memorial Volume,” on occasion of twenty-fifth anniversary of Doctorate of Prof. William H. Welch, M.D., John Hopkins University, 1900. 446 CHRONIC GASTRITIS. ance to disease lessened. It may arise from all processes that lead to venous congestion of the stomach — i. e.> affections of the organs of the portal system, especially of the liver and spleen ; it may also be caused by diseases of the heart. There are certain conditions which may bring about a chronic gastritis by effecting alterations in the composition and structure of the blood ; among these are : anemia, chlorosis, scrofula, secondary anemias following typhus and typhoid fevers, the exanthemata, pregnancy, tuberculosis, dia- betes, gout, and nephritis. Irritating substances brought continu- ously in contact with the mucosa, 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 of alterations in the mucosa itself, such as cicatrices and neoplasms. Our experi- ence is that in the vicinity of such structural changes preexisting in the mucosa there is indeed a gastritis observed, but it partakes mostly of an acute or subacute type. Among the most pronounced causes of the frequency of chronic gastritis are : defective chewing and insalivation, hurried eating and swallowing of large pieces of food, putrefaction of the mouth from carious teeth, or the manifold forms of stomatitis and gingivitis, and, in this country, excessively hasty eating, with the abuse of ice-water at meals and of tobacco and alcoholic liquors between meals. The majority of American people residing in cities live under commercial and social customs pernicious to the digestive organs. Foremost among these con- ditions are the high mental pressure evoked by the demands of business, the constant worry and nervous tension caused by force of competition, the anxiety to get rich rapidly by straining all mental and physical powers ; 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, allowing no time for insalivation. If it were possible, they would gulp the food down dry ; as it will not go down that way, it is washed down with ice-water. Tobacco juice is responsible for much of this disease; also condiments used habitually (pepper, ginger, mustard, horse- radish), and the habitual use of drugs (arsenic, silver salts, iodids). Chronic gastritis is most frequent among habitual consumers of alcoholic liquors. From what was said, under acute gastritis, of the experimental production by Ebstein of this disease with alco- hol, 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 PATHOLOGY OF CHRONIC GASTRITIS. 44 / patient’s indiscretions play a very important role. But, as most persons treat their stomachs badly, and neither eat with proper mastication 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 fiber allgemeine Therapie,” Leipzig, 1885) expresses a sentiment that deserves to be an apothegm : “ Jeder Mensch hat den Magen den er zu liaben verdient ” (“every one has the stomach which he deserves”). It is not intended here to do injustice to a large number of sufferers from weak stomachs who take the greatest possible care to avoid dyspepsia, and, nevertheless, are liable to acute or chronic gastritis. The etiology explains why the male sex is much more frequently affected than the female. The Pathological Anatomy. — The changes are, as in the acute form x most pronounced in the pyloric region, and from here extend to the fundus. The alterations of structure occurring in the course of chronic gastritis present varying pictures, according to the duration of the disease. In the later stages the variations are considerable, since, at this period, the connective-tissue changes may atone time incline to inflammatory hyperplasia ; at another, may show an atrophic character ; again, either the mucosa or submucosa only, or, in other instances, the deeper layers may be involved, with alternating intensity and extent. The inflammatory process is not at all limited to mucoid degeneration and desquamation of the surface epithelium, but preeminently affects the glandular elements and interstitial tissue, whence it attacks the deeper layers of the gastric wall. In early stages there is a general, diffuse redness, due to hyperemia; in later stages this color exhibits a peculiar pig- mentation, 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 caused by blood pigments which have become stored up in the cells and interstitial tissue ; also by blood- corpuscles that have left the vascular channels and undergone pigment metamorphosis during the long-standing chronic hyper- plasia. This pigmentation must not be confounded with post- mortem discoloration. Inflammatory Hyperplasia . — In this form the gastric mucosa may either preserve the velvety appearance peculiar to the normal 448 CHRONIC GASTRITIS. inner surface of the contracted stomach, or it may be covered with irregular warty projections, and exhibit immense development of the pyloric “ plicae villosae.” This is due generally to inflamma- tory infiltration of the interglandular and subglandular connective tissue, but particularly to the same process occurring in the con- nective-tissue ridges (“ Leisten ”) existing between the vestibular entrances to the gland-ducts (“ Vorraume ” of the Germans), or peptic duct alveoli, as we prefer to call them. If these hypertro- phic hyperplastic processes are confined to circumscribed areas, they may assume exaggerated degrees, forming polypoid prolifera- tions which, as a rule, are attached by broad bases ; in conse- quence, however, of connective-tissue contraction, they may also occur pedunculated. In this way papillomatous excrescences may be developed which project into the lumen of the stomach (Orth, “ Gastritis Polyposa,” loc. 710). When the submucosa is attacked with inflammatory infiltration and new formation of connective tissue, the loose tissue is first transformed into one much richer in cells, subsequently into a tougher, more inelastic layer, resulting naturally in a much reduced movability of the mucosa upon its substratum. When this chronic process results in 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 (“ Schrumpfung,” “ cirrhosis ventriculi ” ; “ linitis plastica,” Brinton). In the pyloric portion this process may lead to stenosis. Frequently, the muscularis also is hypertrophied, as a consequence of the chronic inflammation transmitted through the submucosa. This muscular hypertrophy is most pronounced at the pylorus. The localization at the pylo- rus of the maximal intensity of the inflammatory process in the mucosa, submucosa, and the muscularis, makes the origin of a pyloric stenosis in consequence of chronic gastritis intelligible. This kind of stenosis is usually spoken of as benign (hyperplastic stenosis), in contradistinction to the malignant stenosis of car- cinoma (Hemmeter and W. R. Stokes, loc. cit .). Much diversity of opinion 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 its contained lymph- follicles. Rindfleisch maintained that a greater growth of the mucosa than of the submucosa was the cause. Ziegler explained the mucosa polypi by proliferation of the submucosa. Ebstein INFLAMMATORY ATROPHY. 449 assumed an inflammatory hyperplasia of the tissue between the glands. Jones assigned as a cause an excessive contraction of single bundles of the muscularis mucosae. Undoubtedly, this gastritis polyposa, with its mammelonated appearance, may be formed by a great diversity of processes. Inflammatory Atrophy . — The progressive plastic character of the inflammation just depicted may lead to retrograde metamorphosis before it has progressed very far ; in some cases it may not de- velop at all, but the disposition to break down and atrophy may start early in the disease. These atrophic changes are most marked in the glandular elements, and may be limited to these. Some- times the inflammations of the mucosa and gland-cells have, from the outset, a degenerative tendency, and no hypertrophy or hyper- plasia enters into the anatomical picture. The surface columnar epithelium and the cylindrical epithelium of the vestibular alveoli fall prey to a mucoid degeneration and desquamation. The epithe- lial cells of the peptic glands undergo 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 changes go on un- hindered in the submucosa and muscularis; again, the atrophy may extend to the latter layers, and bring about a wasting of all gastric strata. This last condition was formerly designated “ tabes of the stomach ” (the “ phthisis ventriculi ” of Rokitansky). Under these irreparable atrophic states anomalies in the gastric volume may develop, but dilatation is here more frequent than contraction. Atrophy of the stomach may occur without preceding chronic gastritis. It then appears as a simple degenerative process, and follows severe anemic, 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 coexistent anemia, it is sometimes very difficult to decide as to the primary causative disease. In these cases it is well to bear in mind that anemias, even those of a grave pernicious character, may be a consequence of, or rather secondary to, atrophy of the gastric mucosa which has extended to the intestinal mucosa. Our countryman, Austin Flint, was the first to call attention to the relation between anemia and atrophy of the gastric glands. In i860 (“American Medical Times,” i860) he expressed the opinion that some cases of obscure and profound anemia are dependent 450 CHRONIC GASTRITIS. 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, Philadelphia, 1881.) Since Flint’s publications, cases have been reported by Fenwick (“The Lancet,” 1877, July 7th, etseq.); Quinke (“Volk- mann’s Samml. klin. Vortrage,” No. 100, case b ) ; Brabazon (“The British Medical Journal,” 1878, July 27th); Nothnagel (“ Deutsch. Archiv f. klin. Med.,” Bd. xxiv, p. 353); Bartels (“ Berlin, klin. Wochenschr.,” 1888, No. 3); Scheperlen (“ Nordisch. Medic. Arkiv,” 1879, Bd. xi, No. 3); Osier (“ Atrophy of the Stomach, with the Clinical Features of Progressive Pernicious Anemia,” “American Journal Med. Sciences,” 1886, No. 4). Rosenheim re- ported two similar cases which appeared to be pernicious anemia (“Berlin, klin. Wochenschr.,” 1888, Nos. 51, 52). Inasmuch as these cases of atrophy of the gastric mucosa are accompanied by marked changes in the blood, signs of breakdown in the red blood-corpuscles, increase in the white corpuscles, and formation of macrocytes and microcytes, the question may arise whether pernicious anemia is really an independent disease or the result of gastric atrophy. Atrophy of the mucosa — not secondary to well-known stomach or general diseases, but occurring as a primary disease — has been claimed to exist by Fenwick tyoc. cit.). Professor William H. Welch (Pepper’s “ Amer. System of Med- icine,” vol. xi, p. 616), however, was, at the time of that publication, of opinion that the existence of atrophy of the stomach as a primary, independent disease had not been established, the histo- logical examination of many of the cases reported as such having been defective. Professor Welch has since modified his views on this subject. From the statements of some writers the impression might be gained that the hypertrophic hyperplastic form of chronic gastritis was, from its fully developed stage, changed into the atrophic form. This would mean the total disappearance of the papillary, polypoid proliferations of the “ etat mammelone,” because the mucosa of the atrophic form is very smooth. According to Orth (loc. cit., p. 710), this is very improbable. He is of the opinion that the atrophic form is developed uniformly by trans- formation of cellular interstitial tissue into contracting cicatricial tissue, bringing about thinning of the mucosa and degeneration of the glandular elements without the intervening features of hyperplasia above referred to. ULCERATIVE PROCESSES IN GASTRITIS. 45 I Ulcerative processes are said to occur (Ziegler, loc. cit .) when, in the course of the disease, intense (hemorrhagic) inflammation pro- duces necrosis of the epithelium and submucosa, and its subsequent “ sequestration.” In this way the so-called catarrhal gastric ulcers and hemorrhagic erosions are formed, which may be associated with hemorrhage. Cruveilhier (*‘ Anatomie Pathologique du Corps Humaine”) records a follicular gastritis in which ulcers were said to originate in the follicular glandular apparatus. The ulcers of chronic gastritis are mostly small, round, or irregularly indentate. They are supposed to heal and form flat pigmented cicatrices. Forster asserts that they may lead to per- foration. Orth (loc. cit.), whose statements merit confidence because of his scientific conservatism, is of the opinion that ul- cerative processes in the course of chronic gastritis are very rare. The minute anatomy of the process is that of a parenchymatous and interstitial inflammation. The glandular cells are partly de- stroyed, partly granular, and partly shriveled up; differentiation between the chief (Hauptzellen) and the parietal cells (Beleg- zellen) is impossible. In many places, especially in the pyloric region, the ducts have lost their regular order of lying alongside of one another, and show atypical manifold ramification like glove fingers. Isolated glands become separated at the fundus and ap- pear as cysts at the border of the submucosa ; these are either empty, with a smooth lining membrane, or are filled with the re- mains of glistening hyaline cuboidal epithelium. There is an abundant small-celled infiltration which is especially marked near the surface of the mucous membrane ; the cells lie between the glands, and, in places, push their ducts far apart. In the hyper- plastic form we see processes of connective tissue which proceed upward between the glands from the submucosa, like the branches of a tree. The free surface of the glandular layer is covered with a film of mucus inclosing many leukocytes and nuclei (Ewald). The superficial layer of the epithelium of the ‘mucosa is loosened, and can be separated in adherent shreds, which may sometimes be found in the wash-water after lavage of the stomach. In sections one can readily see the mouths of the glandular ducts and the sur- rounding epithelium. The epithelial cells of the vestibular alve- oli (“ Vorraum ”) are, for the greater part, filled with a pale mucous mass, which projects sharply against the lumen without any inclos- ing membrane, as described by Kupffer in the normal stomach. Ewald has been able to study this and the following conditions in 452 CHRONIC GASTRITIS. specimens which were obtained immediately after death, or from living persons after resection of the pylorus. In the conditions (to be described presently) of gastritis mucosa or mucipara, this mucoid degeneration may be observed to extend to the base of the glands, so that in place of the ordinary chief and oxyntic cells, we find only cells in the most varied stages of mucoid degeneration Fig. 34. — Atrophy and Vacuolization of Glandular Elements— Mucoid Degeneration of Peptic Cells — Increase of Interstitial Connective Tissue— Small Round-celled Infiltration. In some places the glandular elements have disappeared, leaving empty, circular spaces. From a case of chronic (alcoholic) gastritis (this fragment was found in the wash-water). (see Fig. 34). This condition is especially marked in the pyloric region. Some isolated cells may be found which are still intact, the mucus filling only a small part of them, while the rest of the cell is occupied by granular protoplasm and a large nucleus. In others, the mucus occupies the greater part of the cells, and crowds the protoplasm and the flattened nucleus against its base. In still SYMPTOMATOLOGY. 453 others, the cell membrane has ruptured, and the mucus has escaped into the lumen of the duct of the gland, where it has been precipi- tated in streaks by the alcohol. This gives rise to very delicate figures which resemble a row of horseshoes with their openings toward the lumen of the gland. That this is really mucus, and not the isolated formation of vacuoles as described by Stohr and Sachs, is easily proved by the reaction with acetic acid, and the grayish color with hematoxylin. Ewald emphasizes the fact that these features are found only where the mucous membrane has been placed in alcohol while still warm ; in old tissues he has never met them. Thus there is a mucoid degeneration of the protoplasm of the cells, which extends deep down into the fundus of the gland. Symptomatology. — As a general rule, the onset of gastritis can not be determined with certainty, because it develops very gradually and insidiously, either as a continuation of acute gastritis and of other diseases, or as an independent disease ; the initial symptoms, not being very pronounced, are generally ignored. Only the sudden aggravation caused by dietetic errors, and other injurious influences, lead to the conclusion that a serious disease is present. The clinical picture varies considerably, although the signs of a disturbed digestion, as indicated by absence of appetite, eructation, nausea, vomiting, pressure and fullness in the gastric region, repeat themselves in various cases ; first one symp- tom and then another will manifest its presence or be entirely absent. Perhaps the most constant of the early symptoms is — Absence of Appetite {Anorexia ). — Even in less serious attacks this symptom, as a rule, exists, and may eventuate in disgust for the customary diet. After prolonged fasting the patient feels that the stomach is empty, but there is no desire to eat and no hunger. There is, however, a strong craving for “ piquante,” salty, or acid food. It seems as if an instinctive knowledge existed that the production of gastric juice is depressed and that the mucosa requires a stronger incentive to secretion. Sometimes a slight appetite is, at rare intervals, developed, which, however, a very few mouthfuls of food suffice to satisfy completely. Incident- ally the desire for food will increase if the patients force themselves to eat; now and then bulimia — an intense hunger — may develop at extraordinary times, — e.g, during the night, — but this is more fre- quent in the neurosis of hypersecretion, which was formerly classed as a gastritis. Thirst and salivation are frequently increased. 30 454 CHRONIC GASTRITIS. Taste . — We have rarely observed a case of chronic gastritis of long standing in which there were not present one or more of the follow- ing complications : Pharyngitis, posterior nasal catarrh, laryngitis, or a form of stomatitis or glossitis, the last occurring most fre- quently. This condition of the mouth perverts taste, rendering it pasty, sometimes distinctly unpleasant, acid, bitter, or metallic: The breath is frequently offensive, caused by caries of the teeth and by decomposition on and in the lingual epithelium, and eliciting the remark that “ food has no taste.” Almost all foods then taste alike. Occasionally, the breath will first become offensive at the height of indigestion, one or two hours after meals, and especially so after ill-smelling eructations ; this is suggestive of gastric de- composition. Nausea is an early symptom, generally preceding emesis ; it may exist by itself for many hours without emesis, and may even occur on an empty stomach. When it occurs after eating, it subsides upon vomiting the food. The ingestion of food may diminish or increase the nausea, which is not always a direct effect of ingesta or fermenting contents on the stomach itself. We have observed it when no food has been taken by the stomach for ten days, when daily lavage has been carried out and nutrition conducted by rectal feeding. This form of nausea may be an effect of intestinal auto- intoxication of a severe type, as these chronic caseT of gastritis are occasionally subject to “ ptomain storms.” Eructation is in all cases present at some time. The gases brought up are air and carbon dioxid ; in some rare instances in- flammable gases, such as hydrogen and marsh-gas, CH 4 , have been eructated (Ewald, Rupstein). The gases may be tasteless and odorless, or may have an offensive after-taste of rancid or bitter character, particularly when small portions of ingesta rise up with the belching. Sometimes the contents of the stomach are very rich in organic acids, this being most likely when the motility and the secretion of normal HC1 are suppressed. A very high total acidity, showing no free nor combined HC1 at all, will then be composed almost entirely of lactic, butyric, and acetic acids. This is a very rare occurrence in chronic gastritis in our experience, and, as a rule, associated with some disturbance of motility. When this acid mass is forced up into the esophagus during the eructations, a very annoying heartburn, or pyrosis, ensues, which seems localized at various parts of the gullet or cardia, and may last for hours. THE VOMITING IN CHRONIC GASTRITIS. 455 Vomiting , though not so frequent as in acute gastritis, neverthe- less occurs quite often. In the chronic gastritis of drinkers it is often a regular event each morning, and is then known as the “ morning vomit,” or vomitus matutinus (water-brash), which Fre- richs attributed to the swallowing during the night of saliva and the secretions from the pharyngeal catarrh. The morning vomit is usually alkaline, as a rule it inverts starch to sugar, and gives the red rhodan-kalium KCNS reaction with chlorid of iron. A tough, glassy, morning vomit occurs in some patients who are not drinkers ; after severe retching, the mucus may be found tinged with blood. We have under observation at present a female patient with chronic gastritis, who vomits this glassy mucus almost the moment she raises her head from the pillow in the morning. Vomiting which occurs after meals brings out food in a more or less partially digested state, according to the duration of its retention in the stomach and the condition of the secretions. The eructated ingesta are imbedded in tough mucus, and may be in a state of fermentation. Bile may form part of the admixture. If the gas- tritis is due to secondary passive hyperemia (“ Stauungskatarrh ”) accompanying hepatic cirrhosis, the vomit may contain blood from the rupture of minute varicosities on the mucosa. The ejected food contains organic acids (particularly after carbo- hydrates have been ingested), but no free acids. We have been struck with the frequency of the occurrence of excessive amounts of acetic acid when the gastritis has been set up by long-standing abuse of alcohol. Yeast cells, sarcinae, and a large variety of bac- teria may be present. With incipient and not very gr^ve cases the ferments, pepsin and rennin, are yet to be detected ; but, in later stages, they are evident only after adding HC 1 slightly in excess of the deficit ; this really shows that the proenzymes, not the per- fect ferments, are present. Finally, pepsinogen and rennet zymogen are absent ; and, in very advanced forms, even the mucus will cease to be secreted. This last symptom is an indication of the com- plete atrophy of the mucosa. The tongue is very frequently coated with a grayish-white deposit, most marked on the back and root of the organ. The impressions of the teeth are retained by it. At the edges and apex the tongue presents a deeper red color, with swollen papillae. The coating may disappear toward evening, to reappear in the morning. Henoch (“ Klinik der Unterleibskrankheiten,” Berlin, 1863, p. 382) holds that the appearance of the tongue is really not always a 456 CHRONIC GASTRITIS. mirror of the stomach, but that its condition is to be regarded simply as an index of the existing state of the oral mucous mem- brane. Certainly the tongue is the more frequent organ of the two to first become diseased, as it is nearer to the outer world and its infections 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 antecedent diseases involving the stomach. Schech (“ Krankheiten d. Mund- hohle ”), in addition to malformations and inherited or acquired defective forms of the mouth, describes 16 distinct diseases of the human mouth, not including neoplasms, tumors, and results of ner- vous diseases. Seifert (Penzoldt and Stintzing’s “ Handbuch der spez. Therapie,” Bd. iv) describes 23 mouth diseases. Kraus (“ Erkrank. d. Mundhohle,” etc., Bd. xvi ; “ Spez. Path. u. Therap.,” von Nothnagel) describes 36 diffuse and 22 partial inflamma- tions of the mouth and tongue. In the primary form all these arise in the mouth, and some occur as secondary forms in acute inflammatory conditions of the digestive tract, particularly after infectious diseases. We have paid particular attention to the state of the tongue, esophagus, 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. A critical review of the etiology of gastric diseases can not fail to evince the fact that the prominent causes can, and most often do, affect the mouth and stomach alike. The gastric disorders in which the tongue is most frequently unaf- fected are those associated with little or no gastric sepsis,/, e ., ulcer, hyperacidity, neurasthenia gastrica ; whereas in diseases asso- ciated 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 not fail to notice a lack of clearness and pre- cision, which doubtless indicates that the relation between remote and local causes is not well understood concerning this matter. A systematic bacteriological and histological study of coated tongues is very much needed in association with gastric diseases. The attempt to establish a definite, characteristic condition of the SUBJECTIVE SYMPTOMS. 457 tongue for every gastric disease has thus far failed. The exten- sion of stomatitis and glossitis to the stomach by the deglutition of infective material is plausible. But the various forms of gas- tric diseases may also extend upward, either by eructations or direct cellular continuity. Then, again, the oral and gastric cavi- ties are in intimate correlation, and may mutually affect each other through the vascular and complex nervous channels. Fleischer ( loc . city p. 820) holds that the importance of the coating of the tongue as a sign of gastritis has been much overrated, and that the tongue may be clean notwithstanding very evident chronic gastritis, and may be coated when this disease is absent. Never- theless, he considers the frequent coincidence of coated tongue and gastritis remarkable, but attributes it to a concomitant stomatitis. General Nutrition . — Chronic gastritis of long standing, left un- treated, will inevitably affect the general nutrition. As von Noor- den repeatedly emphasizes, “ most dyspeptics do not eat enough,” and in consequence of this emaciation ensues to such a degree that even physicians suspect a grave underlying disease (tubercu- losis or carcinoma) where there is only a chronic gastritis. The absence of appetite is most frequently caused by a suppression of secretion of HC 1 . Feeling of pressure and fullness in the epigastric region is, in many cases, complained of, and may be evident on awakening or develop after ingestion of food. The epigastric region in these cases is very likely to be arched forward and outward, and very sensitive to pressure, even the weight of the clothes being annoy- ing. If no dilatation exists, the lower border of the stomach is found in its natural place. It must not be forgotten that a stomach may be dilated considerably and yet the lower border be found in normal position, for the organ may be enlarged upward or laterally, displacing the diaphragm. Professor J. Schreiber, of Konigsberg, has repeatedly called attention to the fact that the horizontal um- bilical line is a misleading landmark by which to judge a dilatation, and that the upper border should, in all cases of suspected dilatation, be determined (“ Archiv f. Verdauungskrankh.,” Bd. 11, Heft 4). It may be possible to ascertain by palpation whether the gastric walls are thickened or not. If a dilatation be present, there exists, gen- erally, a stenosis of the pylorus ; more rarely it is due to so-called atony. The feeling of pressure may increase to a constant dull pain, which should, if it becomes intense, lead to suspicion of car- 458 CHRONIC GASTRITIS. cinoma or ulcer. Some patients with chronic gastritis suffer during digestion from an active peristaltic unrest in the stomach and intestines, their attention being directed to it by abdominal rumbling and gurgling (borborygmus). Conditions of Gastric Contents ; Secretion. — The results of microscopical and chemical analysis after 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 the present state of the disease. Boas recognizes, with regard to these points, four varieties of gastritis, viz. : (i) Acida ; (2) anacida ; (3) mucosa ; (4) atrophicans. The separation of these four types clinically is difficult and has little practical value. In my expe- rience it is sufficient to ascertain whether we are dealing with a simple chronic gastritis or one that has already advanced to atrophy. It is of value to know whether the mucosa is still in a condition of inflammatory irritation, or whether this has terminated in a state of connective-tissue degeneration. The establishing of a separate form of gastritis mucipara, for instance, may have its pathological justification, when one can demonstrate extensive mucoid degeneration of the mucosa, and when there has been an enormous vomiting of mucus in the history of the case. Simple chronic gastritis and chronic gastritis mucipara simply denote differences of degree of the same process. Simple chronic gastritis is also a mucous gastritis. The presence of large amounts of mucus in the empty stomach in the morning is the most char- acteristic symptom of this disease. Gastritis Acida. — State of the Secretions . — Prior to the results of recent investigations, it had been uniformly maintained that ab- sence or great diminution of HC 1 was a constant symptom of chronic gastritis. Boas argues that there is a form of typical in- flammation of the stomach — termed by him “ Gastritis Acida ” — in which there is present an increased amount of mucus, together with a normal amount of acid, or even superacidity (Boas, “ Ueber Gastritis Acida,” “ Mittheil. d. Naturforscher-Versamml. in Wien,” 1894). Even the mucus from the fasting stomach may turn Congo- paper blue. Gastritis Anacida . — In this subdivision free HC 1 is diminished or entirely absent, but combined HC 1 is still present. Egg-albumen discs are but slowly digested, or not at all, in the filtrate, even after addition of HC 1 . The difference between this and the atrophic form TVPES OF CHRONIC GASTRITIS. 459 is but one ot degree, as in the latter all secretion is lost com- pletely. Gastritis Mucosa , or Mucipara . — As was pointed out (page 131) before, when rhinitis, laryngitis, pharyngitis, and bronchitis can be eliminated, large quantities of mucus in the gastric contents, as a rule, speak for chronic gastritis mucosa. The cases not forming much mucus represent end stages of the disease — the atrophy. The mucus-formation can be best estimated by washing out the fasting stomach. There should be no difficulty in differentiating gastric mucus from that derived from the respiratory passages. The former is generally thin, clear, glassy, stringy, and flowing; the latter thick, opaque, yellowish-gray, and lumpy. In the washing from the fasting organ one frequently finds the organic, structural form-elements of the mucosa minutely described in the last chapter and on page 135. If these bits of mucosa are found at repeated washings, showing these elements either in conglomera- tion or singly, there can be no doubt of the existence of glandular chronic gastritis. Frequently the morning contents of the fasting organ show numerous leukocytes. The contents should be drawn by expression ; if possible, without using water. In gastritis chronica mucipara the contents may show a normal amount of HC 1 , or may be either neutral or alkaline. Gastritis Atrophicans . — In this variety both free and combined HC1 are absent, and the tests for enzymes and proenzymes are negative. Milk taken or poured into the stomach is returned mostly in unchanged condition. Martius and Luttke (Joe. cit.) f von Noorden, and others, maintain that absolute disappearance of pepsin and rennin is never seen. From large clinical experience I am prepared to state that the end stages of atrophic gastritis give no evidence of ferments in gastric contents by any of the known tests. Nor would it be rational to suppose that in hypertrophic gastritis, in which the stomach is converted into a hyperplastic, dense, hard mass of muscle and connective tissue, with no histological remnant of a glandular layer, there should be any possibility of the forma- tion of enzymes. In atrophic gastritis, more than in the other forms, there are very characteristic, lancinating pains. The digestion of albumin discs or fibrin in the thermostat is much retarded, or may be wanting entirely, denoting the suppres- sion of the secretion of pepsin. Disappearance of rennin and its zymogen goes on simultaneously with that of pepsin. In cases with loss of rennin the zymogen of 460 CHRONIC GASTRITIS. this ferment must be tested for. Among other observers, Bouveret (“ La pepsine et le ferment lab.,” “ Gaz. Med. de Paris,” 1 893, No. 22) declares that the absence of this zymogen is an important criterion of the degree to which the destructive process has advanced. For the same purpose, Jaworski suggests the introduction of decinor- mal solutions of hydrochloric acid into the stomach, to awaken any slumbering remnants of proenzyme formation and convert them into perfect enzymes. In no case that shows the presence of rennin zymogen need hope of complete or partial restitution be resigned. Age . — This is preeminently a disease affecting adults, for the young are not so liable to abuse their stomachs, or so subject to the manifold factors composing the etiology ; besides, their recon- structive and compensatory powers are greater. The majority of cases are over forty years of age, but Litten (“ Zeitschr. f. klin. Med.,” Bd. xiv, S. 573) has reported a case of eighteen years, and Einhorn one of twenty-one years. The case of Westphalen (“ St. Petersburger med. Wochenschr.,” 1890, Nos. 37 and 38) was, how- ever, verified by autopsy ; it occurred in a young man twenty-eight years old. We have had under our personal observation since 1888 a young printer, at that time in his twentieth year, whose, case showed absence of enzymes and HC 1 , with much mucus. Numerous leukocytes were evident in the contents before food had been taken. Although we have frequently since analyzed his stomach contents, no hydrochloric acid or proenzymes have ever been detected. But on several occasions there appeared fragments of gastric mucosa, showing glandular atrophy and chronic inflam- mation. The condition of the bowels most frequently exhibits constipation. Absence of the antiseptic action of hydrochloric acid favors intes- tinal fermentation, flatulence, and meteorism. When there is much decomposition of ingesta, intestinal irritation will eventually set in, accompanied by diarrhea. The urine is rich in urates and phosphates and often gives a strong indican reaction. The total acidity of the urine is reduced. The general health is variable ; the body weight may either be reduced or remain constant for years : this last indicates that the intestinal digestion is good. Many changes of the general condi- tion, from good to bad and vice versa, may occur, but as the chronic inflammation progresses there are marked symptoms of general dis- comfort and indisposition to bodily or mental exertion. The least MOTOR FUNCTIONS IN CHRONIC GASTRITIS. 46 1 exertion rapidly tires, bringing on pains in the limbs, and despite this exhaustion there may be insomnia. This leads to a depression of spirit which may control the entire mentality, and brings on hy- pochondriasis and melancholia. This leads me to refer to the psychic and nervous symptoms, of which there maybe many, begin- ning with timidity and worry at every new symptom, precordial fear, oppression, and cardiac palpitation accompanied by occasional attacks of dyspnea. The so-called stomach vertigo, first described by Trousseau, I have never observed in chronic gastritis, nor the agarophobia (i. e., terror in crossing wide and empty localities alone) which Fleischer (loc. cit.) says occurs as a psychic accompaniment. From practical observation I am disposed to believe that these psychic and nervous phenomena have been exaggerated, as they •occur only in very protracted cases, and then even inconstantly. Disturbances of Motility . — A great number of cases of chronic gastritis have been examined at the University of Maryland Hos- pital and the Maryland General Hospital, with regard to the peris- talsis ; and, in the large majority, this has been found normal or slightly exaggerated. We use the method described on pages 76- 80. Boas declares that he has never observed a dilatation arise from a chronic gastritis (“ Diagnostik u.Therap. d. Magenkrankh.,” 2d edition, p. 21). It is evident that stenosis of the pylorus can occur which is not caused by cicatricial contraction nor by neo- plasm, but by hyperplasia of the muscular sphincter of the pyloric region. If a chronic gastritis lasts long enough, it is a fair pre- sumption that it may result in a gastrectasia due either to atrophy of the muscularis from connective-tissue invasion, or to the muscular hyperplasia, producing a stenosis. Boas has also con- clusively shown that lactic acid is not, as a rule, formed in glandular gastritis. Complications. — The most frequent is the extension of the in- flammation to the intestines. The frequent association of chronic duodenitis with the disease explains the occurrence of catarrhal icterus, which is an extension of the intestinal inflammation to the gall-ducts. The results of chronic gastritis are, in protracted cases (particularly when the intestines have been involved), marked dis- turbances of nutrition and anemia, which, as we have had occasion to observe, may assume very serious forms. The duration may vary from several months to years, particu- larly if the patients have not the means nor the will-power to follow dietetic regime. 462 CHRONIC GASTRITIS. Atypical forms of chronic gastritis are by no means rare occurrences, and sometimes make a clear diagnosis very difficult. In the foregoing description of the disease the lack of very charac- teristic and peculiar symptoms is evident. In addition to this, the symptoms of loss of appetite, pressure, fullness, eructation, vomit- ing of mucus, may be absent in atypical forms, and it has been observed that chronic gastritis may run its course in a latent, unde- tected manner. Again, it may exist under the manifestations of a nervous dyspepsia, or there may be such prominent intestinal symptoms as to disguise the gastritis. Diagnosis. — It requires careful study not only to distinguish chronic gastritis from other diseases, but also to distinguish the simple, mucous, atrophic, and chronic gastritis acida (of Boas) from one another. 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 estab- lished after the possibility of the existence of other affections of the stomach has been excluded. This disease may strikingly resemble the clinical pictures of the gastric neuroses, of ulcer, and even carcinoma. Dilatation is a very rare complication, and therefore not a confusing factor in diagnosis. One should not make the diagnosis definite at the first examination, but reserve opinion until the patient has been studied during three or four visits. It has, in some cases, taken a much longer time than that to obtain satisfactory evidence of the disease. The best evidence is afforded by repeated microscopical and chemical examination of the wash-water and test-meals, and the persistent presence of much mucus in the empty stomach. It will be necessary to dwell upon the differential diagnosis be- tween chronic gastritis and the neuroses, ulcer, carcinoma, and amyloid degeneration : The neuroses may present all the symptoms of a chronic gastritis, particularly the absence of HC1; but, after patient and repeated test-meal analysis, it will be found that the neuroses will some day show a normal and even excessive amount of HC1. The course to pursue is to wait for this evidence. The presence of much mucus, epithelial cells, and leukocytes in the wash-water from the jejune stomach indicates chronic gastritis. Demonstration of enzymes and proenzymes is very valuable, as a normal amount of pepsin and rennin (when HC1 is absent) speaks for neurosis and against gastritis. In the absence of HC1, DIFFERENTIAL DIAGNOSIS. 463 Jaworski’s method ot pouring in decinormal HC1 should be used to stimulate the formation of enzymes. In the incipient stage of chronic gastritis the enzymes may be present, even in normal amount ; but they disappear gradually as the disease progresses. By the time the physician is consulted, the enzymes are very much diminished or entirely absent; this is an indication of an inflammation of the mucosa, 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 chronic gastritis. The ulcer-pain is localized, well circumscribed, very intense, and occurs at definite times after partaking of food. Hematemesis, of course, points to ulcer. The vomit of ulcer shows hyperacidity, which is, as a rule, absent in gastritis. In atrophic gastritis there may be lancinating pains, but they are diffuse and not so frequent or constant as in ulcer. From carcinoma the differentiation may be difficult when no palpable tumor can be detected. This is intelligible when one re- flects that carcinoma is generally complicated with chronic gastritis. If a pyloric carcinoma be present, the most noteworthy symptoms are : stenosis, motor insufficiency, and stagnation of food with large amounts of lactic acid. A carcinoma seems to strike a stomach suddenly with very severe symptoms and general disturb- ances — pain, emaciation, and vomiting; whereas chronic gastritis is characterized by slow increase of the gravity of symptoms, with alternating improvements and aggravations. It is an important fact that the motility is not disturbed in chronic gastritis, and, therefore, the stomach rarely contains anything but mucus, iso- lated cells, and leukocytes. But in carcinoma the peristalsis is seriously impeded from the onset, and therefore there must be stagnation, retention, and acid-fermentation. These products of retained ingesta occur even when there is no stenosis of the py- lorus, as a result of carcinomatous invasion of the muscularis. Gas- trectasia is an exceedingly rare result of gastritis, and can occur only from hyperplastic thickening of the pylorus, a thing seldom reported in the literature of this subject. As stated before, the presence of marked amounts of lactic acid is not observed in gas- tritis, but in carcinoma its occurrence is very frequent. Organic acids are rare in the test-meals of gastritis, whereas in carcinoma there is, as a rule, an excess of lactic and fatty acids early in the disease 464 CHRONIC GASTRITIS. (Boas. loc. cit.). For further differentiation see article on Car- cinoma. Amyloid degeneration of the stomach may lead to complete suppression of the gastric secretion, but it is always a secondary disease, occurring in the sequence of chronic suppurative pro- cesses and pulmonary tuberculosis. If the existence of amyloid de- generation can be established in the spleen, kidneys, or liver, we are justified in considering a secondary involvement of the stomach when HC1 secretion has been proven to be lost. This form of degeneration in the stomach is, in my experience, extremely rare. Synopsis of diagnostic points in various types of chronic gastritis : Contents of Fast- ing Stomach. Acidity. Ferments. (1) Simple Chronic Gastritis. Subacid or anacid. Limited amount of watery mucus; leukocytes ; epi- thelial cells; round cells. Variable^; free HCl rarely present, but if present, lessened in amount ; com- bined HCl present. Pepsin and rennin pres- ent in small amount ; propeptone formed in the stomach. (2) Chronic Mu- cous Gastritis. Much mucus ; epi- thelial fragments. At the beginning there may be a normal amount of combined HCl; later on the amount is low; HCl ab- sent ; HCl deficit. Pepsin absent ; rennin absent; both proen- zymes present ; ex- perimental digestion occurs on supplying the HCl deficit. (3) Chronic Atro- phic Gastritis. Lancinating pains present in this form. Empty; no mucus. HCl absent; HCl deficit ; no com- bined HCl. No enzymes ; no pro- enzymes ; no curd- ling of milk on add- ing HCl. (4) Acid Gastritis. Much mucus ; giving HCl reaction. Normal amount HCl, or hyperacidity. Ferments increased. Prognosis. — Chronic gastritis is a tedious, but not a very seri- ous, affection, as many cases recover under suitable treatment. The prognosis must vary with the stage of the disease as presented, and the intelligence and will-power of the patient. Patients who will study to avoid further detrimental influences, and who have the determination to carry out the dietetic and hygienic manage- ment, will recover. With incorrigible eaters or drinkers, who re- transgress against their stomachs on the slightest improvement, permanent recovery is doubtful. After the establishment of partial or complete atrophy of the glandular mucosa, perfect recovery is impossible ; but as it is well known that a good state of general TREATMENT. 465 health may be maintained with complete suppression of the gastric juice, provided the intestines still function normally, atrophy of the mucosa does not necessarily imperil vitality. On the other hand, there are numerous well-authenticated observations (see literature) that demonstrate severe disturbances of nutrition, particularly per- nicious anemia, as a consequence of gastric atrophy. The instances of complete extirpation of the stomach — Brigham in this country, whose case has already lived longer than Schlatter’s case in Zurich — show that metabolism and nutrition may, for a time at least, be apparently normal with total absence of the stomach. These pa- tients remain under constant medical control, however. Fenwick (loc. cit .) suggests that this pernicious anemia may be due to auto- intoxication from the stomach. Other authors, again, hold that the anemia maybe the primary factor, and bring about the atrophy of the mucosa. This entire question still partakes of a speculative nature, since exact and logical experiments and deductions are wanting. Treatment . — Prophylactic Treatment . — The prevention of the development of the disease implies avoidance of the causes given under the head 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 diseases, must be carefully treated in order to prevent its transition into the chronic form. Explicit directions regarding diet and mode 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 disturbances of appetite and impairment of digestive powers must inevitably render the fundamental disease more serious. The chief predisposing factors to secondary chronic gastritis are passive congestion and accumulation of injurious metabolic products in the heart muscle, with renal insufficiency. In cases of cardiac insufficiency with threatened passive engorgement, digitalis should be used early. One should not hesitate to give digitalis on account of the occasional appetite-disturbing effect of the medicine, as this is usually transient ; an improvement of the appetite and of nutrition in general will be observed in these cases if the treatment be continued; we usually combine it with large doses of strychnin. 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 administration of digitalis, it is expedient to give the 466 CHRONIC GASTRITIS. remedy at the outset of the slightest disturbance of appetite, since our experience has taught us that this will unfailingly become aggravated by delay in the use of the heart tonic. If the stomach rebels against the remedy, the infusion should be given by enema into a rectum previously cleaned by warm normal salt irrigation, or digitalin injected hypodermically. Lavage . — When it is no longer possible to remove the causes that lead to a chronic gastritis, we may yet be able to remove those that maintain or aggravate the malady. These causes are : the accumulation of mucus, and the mechanical as well as chemi- cal irritation of the stagnating contents, particularly when atony and hypertrophic stenosis exist. To accomplish this, emetics are impracticable, because they rarely effect a thorough cleansing, and may increase the inflammation by the convulsive contractions they excite and by their direct irritation. Purgatives are even more deleterious, for several reasons : first, they also increase gastric irritation; secondly, they can not be used habitually; and, thirdly, they hurry decomposing masses into the intestines, there- by precipitating an involvement of this tract and the dangers of intestinal putrefaction and auto-intoxication. Lavage is the only correct procedure in chronic gastritis whenever increase of mucus, absence of HC 1 , decomposition, and a protracted stomach diges- tion are evident. The mucus often adheres very tightly to the gastric walls, since it only 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. f lying on his back, rising or turning on his side — during the lavage ; or by employment of gastric massage. The solution of the mucus is effectually accomplished by adding one tablespoonful of salt and two tablespoonfuls of sodium bicarbonate or biborate to a liter of warm water. To disinfect the stomach after the removal of mucus and fermenting ingesta, the following remedies are approved aids : Salicylic acid, 1 : 1000; thymol, 0.5 : 1000; boric acid, 10: 1000; chloroform water, 5 to 10 : 1000; shake the chloroform with the water, and, after settling, pour off the water, using only the latter; hydrochloric acid, 6 : IOOO; re- sorcin resublimate, 10 : 1000; benzol, 5 : 1000. The solution must be prepared immediately before the 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 two or three days ; others require it twice in twenty-four D I ETETIC TREATM ENT. 467 hours; usually, once a day is sufficient. The time of the washing should be so selected that the exhausted stomach may enjoy the longest possible rest. For this purpose six o’clock in the evening is most suitable, as it is then about six hours after the main meal of the day, and no food or only very light diet is taken after the lavage and before bedtime. In other cases this hour may be in- convenient, and an early hour before breakfast must be chosen. A plan useful in many instances in which the stomach requires rest is to give a fair breakfast at 9 A. m., dinner at 3 p. m., no supper, and lavage at 9 p. m. Washing out the stomach is advisable only when there is much formation of mucus and when there may be stagnation of food. In atrophic or chronic gastritis without much mucus, frequent lavage is not necessary. In these cases the stomach-tube is recommended, not to remove fermenting ingesta or mucus, but to treat the mucosa directly, to stimulate its slug- gish secretion by irrigating with decinormal solution of HC 1 ; if enzymes are still to be detected, common salt solutions are useful for this purpose (about one tablespoonful to the quart). Solutions of NaCl must not exceed the strength of one per cent., as solu- tions of four per cent. NaCl check the HC 1 secretion and are avail- able in the treatment of hyperacidity. (See “Achylia Gastrica.”) Dietetic Treatment . — In each case it is advisable to give the patient a written diet-list, based upon a chemical study of the indi- vidual’s digestive power. Sometimes it will be impossible to give a diet at first that will at the same time suit the patient’s palate and digestive power. The most digestible food will at times disagree with chronic gastritics, and food which would seem a priori very indigestible, agrees well. A good plan is to inquire minutely into each patient’s accustomed diet and ascertain what food especially disagrees. At the beginning, the diet should be of a light kind : one that makes but slight demands upon the working capacity of the stomach. As the motility is good in this trouble, the diet, as far as possible, should be liquid or semiliquid, and in some cases four to six small meals a day are preferable to three large ones. In others it will be insuring rest to the stomach to give only two meals a day, excluding the supper. Nutritious soups, such as beef bouillon enriched by the addition of butter, eggs, beef- meal or jelly, somatose, or nutrose, are generally well borne, but as a rule do not suffice to maintain strength and body weight. It is well to insist on slow eating, thorough chewing, and insalivation as important. The teeth should be looked after, and, if necessary, 468 CHRONIC GASTRITIS. repaired, or artificial ones provided. Should there be a normal amount of HC1 and pepsin secreted, then a diet rich in proteid will be advisable. Suitable articles of diet are all white meats, fish, and eggs, properly prepared ; which means that the roast or broiled meats, even after they are on the table, must be very finely divided on the plate before placing in the mouth. Light vegetables are permissible in form of purees, viz. : potatoes mashed in milk, peas or beans driven through a sieve, spinach, etc. When the HC1, although present, is considerably reduced, the diet will be similar; but spices and well-salted food are more adapted. If the secretion is completely suppressed, it is not expedient to greatly restrict the diet, as these patients are more liable to suffer from inanition. The greatest care is to be employed in the preparation of the food, which must be presented in an appetizing and finely divided form. All meats and fish must be prepared in the steam broiler, and, if needed, they should be previously minced and then reformed into any desirable shape, held by a supporting substance such as ex- perienced cooks are familiar with, generally consisting of bread- crumbs, eggs, salt, and butter. Milk, if it agrees well, is a valuable adjunct to the diet, and even if not well digested, or if there is an aversion to it, should be surreptitiously added to soups, chocolate, rice, sago, gelatins, and farinaceous foods. When it is thus mixed with other foods it is generally very well digested, and adds to their nourishing quality. Von Mehring has recommended a choco- late (Kraftchocolade) which contains 20 per cent, of fat ; it is very palatable and usually causes no digestive distress. When there is emaciation, we give small amounts of alcohol, upon the authority of Chittenden’s experiments that alcohol up to three per cent, favors proteolysis and amylolysis, and is a fat-sparer. If we are sure, from test-meals, that there is no gastric fermentation, — and according 'to our experience there rarely is in chronic gastritis, — we recom- mend the genuine Oporto, Malaga, or imported Hungarian Tokay wines.* When it is evident that the gastritis was caused by bacchanalian excess, it is, naturally, a good plan to exclude alcohol as far as possible. Indeed, when the emaciation is not marked, or when, after a trial, the collective symptoms appear to become worse, alcohol is best avoided. There are, how- ever, cases of distinct alcoholic gastritis in which, after well- observed test-meals, the proteolysis is carried on better when J. Palugyay & Sons, Pressburg. DIETETIC TREATMENT. 469 wine is taken.* The wines we have recommended have not only a stimulating, but, on account of their large percentage of grape-sugar, a nutritive, value. This grape-sugar will, however, increase the lactic acid formation if it be already present. In this last case a standard champagne — Mumm’s Extra Dry, “ Roederer,” Piper-Heidseick — is preferable. Beer and claret are, according to our experience, rarely well borne, and frequently augment gastric distress. In cases of marked anorexia a palatable dilution of brandy or whisky, taken half an hour before meal-times, very often pro- duces an appetite. The so-called “ Angostura Cocktail ” is some- times useful to sufferers from anorexia, but must not be allowed to alcoholic cases. The physiological reasons for the administration of alcohol are explained in the chapter on The Dietetics of Alcoholic Beverages (also in the “ Dietetic and Hygienic Gazette,” May, 1896, p. 289; and R. H. Chittenden, “ Amer. Jour. Med. Sciences,” Jan. to April, 1896, “Influences of Alcohol on the Chemical Processes of Digestion”). Constipation in chronic gastritis should always be treated diet- etically, never by medicines per os. A glass of cold water, or, preferably, of Bedford Magnesia Spring water, before breakfast, is a simple thing, and yet, if persisted in, very often gives an evacua- tion. The breakfast should contain honey, milk-sugar or levulose, some plum, fig, or prune preserves, and Graham bread. Twice daily a glass of buttermilk or kefyr may be administered, if agree- able to the patient. When the constipation resists this diet at the beginning, a trial for the first week should be made with large colon irrigations, with one liter of normal salt solution introduced in the knee-elbow position. Fleiner’s enemata of 250 c.c. ( y 2 pint) of pure olive oil are more lasting in their effects, one enema sometimes keeping the bowels regular for a week. When diarrhea is present, large irrigations of warm water, by removing fermenting and putre- factive colon contents, frequently cure it without other medication. But strict dieting for a few days is always advisable in exhaustive diarrheas, as it shortens the attack. In diarrheas, as well as in con- stipation, the state of the gastric secretion must be regarded, and HC 1 or alkalies must be supplied, as the case may be. Excess of HC 1 secretion may provoke diarrhea by causing carbohydrate indi- * The “rationale” of the administration of alcohol is governed by its effects on the gastric digestion as observed in test-meal analysis — if it impedes digestion it must be forbidden. 31 470 CHRONIC GASTRITIS. gestion. A diet of Pasteurized milk and some stimulant, as brandy, and, perhaps, albumin water for forty-eight hours, to the exclusion of everything else, is most effective. Soup made of bouillon and thickened with wheat-flour toasted brown in hot butter, is quite binding. “ Eichelcacao,” a palatable German preparation of choc- olate, can be recommended for its constipating effect, as it contains much tannin. For special full diet-lists and further dietetic directions concern- ing this disease, as well as other recipes, we refer to the section especially devoted to this subject — the chapter on Dietetics (pp. 223-226). As Gilman Thompson points out, there are some persons in whom the digestion of salt and smoked meats seems to be more easily accomplished than that of prepared fresh meat. Nicmeyer offers the explanation that these preparations are less likely to de- compose in the stomach. As a rule, there is very little fermenta- tion and formation of organic acids in chronic gastritis. After carefully observing this point, we maintain that it is not necessary to withhold the saccharine and farinaceous foods, as Gilman Thompson suggests ( loc . cit., p. 508). On the contrary, they should be liberally supplied, as amylolysis progresses rapidly in stomachs that secrete no HC 1 , and test-meals in my experience do not, as a rule, show the excess of organic acids asserted by von Leube, Ewald, and Rosenheim. Balneological . — There is much truth in what Prof. Ira Remsen said when he opined that the effect of the use of natural or mineral spring waters was not attributable to the chemical constituents or salts of these waters, but more to the favorable mode of life, the better diet, the greater introduction of plain water into organisms which previously received very little of it, and, lastly, to important psychic influences. To these may be added the perfect rest, com- fort, and auxiliary methods of treatment employed at the springs. Thousands of Americans visit the German, Austrian, and French spas annually, when they might have almost the same waters — and sometimes much better ones — in their own country.* Obser- vations are very numerous on the treatment of chronic gastritis by mineral waters, but are rather inexact and based upon imperfect * In extended travels through our Eastern States, I have visited 20 mineral springs discharging very palatable — sometimes carbonated — waters that are not at all known except to people living in the immediate vicinity. MINERAL WATERS, BATHS, GYMNASTICS. 47 1 histories, as many cases are called chronic gastritis which, in fact, do not deserve the name. One can not well judge of the effect of the waters alone, as they are always combined with dieting. The systematic drinking of alkaline waters must not be estimated to be worth more than that of a poor substitute for lavage. As the ob- ject is to promote the solution and evacuation of mucus, all waters will be equally serviceable, even ordinary spring or hydrant water. The salts can be added to imitate the real composition of the famous springs, and are made by several wholesale manufacturers of effer- vescent salts for this purpose, so that the poorer patients may have the effect of mineral springs at home. (For the effects and contraindications of mineral waters the reader is referred to the section on Mineral Springs. The compo- sition of artificial Carlsbad salts is given on pp. 335 to 336.) In the use of alkaline chlorids it is expected to stimulate the secretion of HC 1 . Hot spring waters must be cooled, and the cold water warmed ; and in dilatation and atony, the patient had best abandon the use of water in this manner entirely. Baths . — As in chronic gastritis the general metabolic processes are much depressed, a cold sponge-bath taken before breakfast will gradually make the dyspeptic more resistant by its stimulation of cellular oxidation and its hardening effect. Warm baths we advise, for purposes of cleanliness only, once or twice a week. Gymnastics . — All patients with chronic gastritis should be en- couraged to take moderate exercise : walking, bicycle riding, horse- back riding; also rowing and swimming. A pair of four-pound dumb-bells for men and two-pounders for women should be used three times daily, each time for five minutes, with three minutes of rest intervening between the five minutes of exercise. This will make fifteen minutes of training, and should be done before dressing, in the undergarments, immediately after the cold sponge bath. Great care should be bestowed upon the tonicity of the abdominal muscles. Loss of the unconsciously and continuously acting tonus of these muscles is a most potent factor in the etiology of dilata- tion, gastroptosis, and floating kidney. There are, of course, other causes ; but even if the attachments of an organ are loosened, it can not wander far from its normal location with a vigorous, unrelenting, external abdominal wall. Therefore, all patients subject to digestive diseases, except ulcer and carcinoma, should train their abdominal muscles and keep them active. San- 472 CHRONIC GASTRITIS. dow’s directions for accomplishing this, as described in his book, are excellent. Rest. — When the patient has lost weight and becomes emaci- ated, gymnastics are out of place ; then an absolute rest cure is peremptory. Electricity . — The faradic and galvanic currents are useful in the treatment of chronic gastritis. The former may be used as general external faradism, which is one variety of a general massage. One pole, in shape of a broad, flat electrode, is moved slowly up and down over the spinal column, while the other is moved over both arms and limbs, and particularly over the abdominal muscles. With one pole over the spine, and the other over the epigastrium, the current appears to go directly through the stomach, and yet there is no evidence that the organ does contract. In this case it is doubtful whether any current reaches s the stomach at all. There is as yet no satisfactory explanation of how the good effects ob- served after this method are brought about. However, they may, perhaps, be largely attributable to the abdominal massage and the psychic influence. For the intragastric application of both the faradic and galvanic currents, the practical intragastric electrode of Einhorn is possibly the most convenient. The secretion of gastric juice can not be influenced by either the faradic or galvanic cur- rent, nor can the motility be enhanced (J. C. Hemmeter, “ New York Med. Journal,” June 22, 1895, p. 769). As the currents usually employed for this purpose are too weak to effect a con- traction of the muscularis, Meltzer (“New York Med. Journal,” June 15, 1895) holds that percutaneous and direct faradization of the stomach and intestines can not produce any contraction of these parts. Max Einhorn (“ Archiv f. Verdauungskrankheiten,” Bd. 11, S. 454), in his recent contributions to the subject, is of entirely opposite opinion (see part 1, p. 60). As Ziemssen (“ Elec- trizitat i. d. Medizin,” 1887, p. 445) has emphasized, it is not neces- sary to effect gastric contraction in order that electricity should prove beneficial. In fact, it would appear that a neurometabolic or neurotrophic effect of electricity is becoming more and more under- stood, so that the faradic and galvanic current should be employed, both externally over the spine and epigastrium, and internally with the intragastric electrode ; not because of any undeniable evidence that it can influence secretion, motility, or absorption, but because of the general uniformity of opinion among experienced clinicians that chronic gastritis is undoubtedly benefited by electrical treat- MEDICINAL TREATMENT. 473 ment. Even Goldschmidt (, loc . cit), whose results regarding the effect of the faradic and galvanic currents on secretion and motility- are entirely negative, admits that these are useful agents in the treatment, even benefiting stomach diseases depending upon organic changes. It is evident that while experimental evidence of the manner in which electricity acts on the stomach is neces- sary, the clinical approval of its therapeutic utility is more important. Medicinal Treatment . — Two chemicals seem to have maintained their reputation as being able to benefit the disease; these are ar- Fig. 34A. — Connective-tissue Hyperplasia Separating Remnants of Glands which Show a Small Nucleus Surrounded by a Thin Shell of Protoplasm.— {From the Author's Clinic , University of Maryland .) X 70 diameters. gentic nitrate, either in form of gastric spray (i : 1000) or lavage (1 : 2000), or in form of solution, 0.3 to 120 of peppermint water; of this, one tablespoonful three times daily, on an empty stomach. The second drug is bismuth subnitrate, recommended by Penzoldt (loc. cit.) y Fleiner (loc. cit), and Pick (loc. cit.) in large doses, 4 to 6 gm., in wafers. With both remedies we have had experience, and prefer the latter, together with bismuth subgallate, because it certainly diminishes the amount of mucus formed in alcoholic gastritis : 474 CHRONIC GASTRITIS. R . Bismuth subnitratis, Bismuth subgallatis, Fiant pulv. No. xxiv. SiG. — One powder in a wafer four times daily Unfortunately, this treatment is constipating, and must, there- fore, be combined with a diet promoting evacuation and the use of Saratoga Congress water. Argentic nitrate is best employed in form of the intragastric spray or in the lavage. These drugs are permissible, particularly when diet and massage can not be properly carried out. They were originally suggested for the treatment of ulcer ; their efficacy in some cases of chronic gastritis 48 gm. 3 xij 16 gm. giv. M. Fig. 34B. — Detachment of Remnants of Secretory Cells Containing Vacuoles from Lumen of Peptic Duct.— {From the Author's Clinic , University of Maryland.) X 325 diameters. is, however, undoubted. The bismuth subnitrate and subgallate may be applied by means of an intragastric powder-blower. By the use of the fluoroscope and X-rays it is demonstrable that the entire stomach can be coated in this way. The Hygiene of the Mouth . — The frequent association of stomati- tis, gingivitis, and glossitis with this disease make it all-important that the mouth should be in a healthy condition. Dental defects and their repairs have already been referred to; but, in addition, the mouth should be disinfected after each meal. After removing TREATMENT OF SPECIAL SYMPTOMS. 475 the food debris by toothpick and brush, one of the following anti- septic lotions should be used, both on the brush, applied to the teeth and the root of tongue, and as a mouth-wash : R. Acid, thymol, 0.25 gr. iv Acid, benzoic., 3.0 gr. xlv Tinct. eucalypt., 15-0 f^iiiss Alcohol, 100.0 f^iiiss 01 . menth. pip., 0.75 ffbxij. M. SiG. — Pour sufficient into ]/ 2 of a glass of water until turbidity results. If much decomposition be present, 0.8 hydrarg. bichlorid. corrosiv. may be added. R . Spirit, lavandul. , Spirit, myrciae, aa 50.0 f g xiiss Tinct. myrrh. 5.0 f^j Saccharin, 1.0 gr. xv Menthol 1.0 gr. xv. M. SiG. — One-half to one teaspoonful to a glass of water. Treatment of the Symptoms . — This is of subsidiary importance to systematic treatment by diet, hygiene, and lavage ; but in cases that have progressed too far, or in secondary forms that are incura- ble (albuminuria, diabetes, etc.), a special therapy for symptoms may be indispensable. The treatment of loss of appetite which we advocate is the follow- ing : Lavage with chlorid of sodium, §ss to the quart or a decinor- mal solution of HC1 ; fluid extract of condurango in doses of 5j ; tincture or elixir of gentian. Lavage with quassia, Colombo, or calisaya solutions will often produce appetite. Orexin, a stimulant to the appetite and HC1 secretion (first recommended by Penzoldt), is best given in the following form : R. Orexin, basic, 0.2 gr. iiiss. SiG. — Make one wafer. Take one wafer in a cup of bouillon half an hour before meals, t. i. d. Our favorite tonic for anorexia in chronic gastritis contains strychnin and hydrochloric acid in the following proportion for adults : R . Strych. sulphatis, 0.02 gr. Acid, hydrochlorici dilut., 19.4 f^v Elixir gentianse, q. s. 180.0 f^jvj. M. SiG. — f.^ss in ij aquae after meals, through a glass tube. Fluid extract condurango f^xij may, if desired, be added. Some old gastritics can not tolerate so much hydrochloric acid. Then the dose must be reduced to five drops, t. i. d. Always precede the administration of H Cl by a test- meal analysis, so as to find out the degree of HC 1 deficiency. Pyrosis and eructation are best treated with magnesia and sodium 476 CHRONIC GASTRITIS. bicarbonate, according to the principles laid down in the manage- ment of hyperacidity. Pain . — If diet and lavage do not relieve this, it is best to subject the patient to a rest cure of eight days, with hot external fomenta- tions to epigastrium. The galvanic current has been a very reliable means of easing pain in this affection. Opiates and other narcotics must be avoided ; but, in the very rare cases where this is impossible, they should be given by the rectum or (morphin) hypodermically. The same treatment applies also to vomiting, which is, as a rule, relieved by diet, lavage, small pieces of ice, or champagne ; very rarely does it become so distressing a symptom as to require a hypodermic injection of morphin. Spraying the stomach with menthol and cocain in weak solutions relieves vomiting when lavage has failed. Deficiency of gastric juice and ferments may be supplanted by the use of HC1 internally, as per formula stated above. If HC1 is no longer tolerated, it is well to convert the entire gastric chemistry into an alkaline proteolysis by pancreatin and bicarbonate of sodium. In long-standing cases the mucosa acquires a strange hypersensitiveness to all acids, which points the way to this plan of treatment. Reliable pancreatin and sodium bicarbonate, of each five grs., are recommended by Boas, Witte, Simon, Schering, and Penzoldt. In our private sanitarium we have, by a study of test- meals, found Reichmann’s preparation of fresh ox pancreas an effective digestant. It is made by finely mincing one ox pancreas and extracting it with 15 per cent, alcohol or brandy for forty-eight hours, and straining. The dose is a wineglassful after meals. We very rarely found it necessary to give pepsin ; for if HC1 is still secreted, pepsin will be found also, and if HC1 be absent, although the ferments may be wanting, it is expedient to give only the acid, as proteolysis is sufficiently effective in the intestine, and the effect of the HC 1 is to improve the appetite and prevent intestinal fer- mentations. Motor insufficiency is, fortunately, a very rare occurrence in the disease, but, if present, may be met with use of lavage, electricity, hydrotherapy, massage, and strychnin. This will be more fully treated in the section on this defect. Psychic depression may, according to the most prominent under- lying cause, require one or several of the methods of treatment mentioned. But regular bowel movements, electricity, a daily ADVANCED CHEMICAL AND MECHANICAL DEFECTS. 477 tepid or cold sponge bath, moderate exercise, massage, surf baths, and climatic changes are the most reliable means to be employed. Some of these cases will not recover until brought to a properly managed sanitarium for digestive sufferers. Advanced Chemical and Mechanical Defects . — When the glandular elements have been completely destroyed as a result of hypertro- phic or atrophic metamorphosis of the mucosa and degenerative processes in the muscularis, and also of cirrhotic contraction of the stomach, secretion, absorption, and motility no longer exist. The gravest defect is the loss of motility. For, in the total absence of all gastric digestion, no food except a small fraction of the car- bohydrates (ptyalin) enters into solution. The ingesta are not re- duced sufficiently in size, because there is no churning peristalsis and no secretion ; they are not evacuated into the duodenum, be- cause the propelling peristalsis is missing. Now, although there is no stenosis of the pylorus from cicatricial contraction or neoplasm, we have seen such cases in which there was not even a pyloric hyperplasia. Under these conditions there is what we may term a “ relative pyloric stenosis that is, the pylorus is relatively too small and peristalsis too defective for the passage of the insufficiently macerated ingesta. This combination of things may occur in the last stages of chronic gastritis accompanied by the clinical aspects of progressive anemia, due to inevitable malnutrition, and may sim- ulate carcinoma. Operations have been undertaken, in the author’s experience, where the markedly thickened, hyperplastic muscularis gave the impression of a gastric neoplasm, and the exploratory in- cision revealed the effects of a chronic hyperplastic gastritis. The intestine, although it may be healthy, can not supplant the absent digestion of the stomach by its vicarious action, since it gets no chance to do so, the gastric contents fermenting, and eventually being expelled by emesis, rather than propelled into the duodenum. This state should be treated exactly as if there were a real pyloric stenosis, namely, by operation, — either by gastro-enterostomy or by dilatation of the pylorus ; or, if an excessive atonic gastrectasia with immense enlargement of the stomach and normal pylorus be present, by gastroplication (Bircher). So far it appears that gastro- enterostomy has been done but once under these conditions for typical gastric atrophy (Westphalen, “Petersburger med. Wochen- schr.,’’ 1890, 37, 38) occurring in a tuberculous patient. As the expelling force of the peristalsis is much reduced, gastro-enteros- tomy will probably be preferable to dilatation of the pylorus. The 478 CHRONIC GASTRITIS. indications for surgical operations upon the stomach have been separately considered (p. 348). LITERATURE ON ACUTE AND CHRONIC GASTRITIS. In addition to the text-books of — Debove and Remond, Eichhorst, Niemeyer, Einhorn, Ewald, Orth, Fleiner, Fleischer, Oser, Martin, Sidney, Forster, Penzoldt, Bamberger, Henoch, Pick, Birch-Hirschfeld, Jiirgensen, Riegel, Boas, Kunze, Rokitansky, Bouveret, Lebert, Rosenheim, Brinton, Leo, Striimpell, Cohnheim, Leube, Trousseau, Cruveilhier, Liebermeister, Wegele, Dujardin-Beaumetz, Hayem, Ziegler, and others. 1. Aaron, C. D., “Chronic Dyspepsia,” “Trans. Mich. Med. Soc.,” Grand Rapids, 1898, 281-291. 2. Beaumont, “Experiments and Observations of the Gastric Juice and the Physiology of Digestion,” Combe’s edition, 1833. 3. Benedict, A. L., “ Some Thoughts on Subacute and Chronic Gastritis,” “Medicine,” Detroit, 1897,111, 353-359. 4. Boas, J., “ Ueber Schwefelwasserstoff bildung bei Magenkrankheiten,” “ Centralblatt f. klin. Med.,” 1895. 5. Cahn, A., “ Die Verwendung der Peptone als Nahrungsmittel,” “ Berlin, klin. Wochenschr.,” 1893. 6. Cagigal, A. O., “Um caso'de gastrite chronica e arterio esclerose com- modificacoes nervosas perephericas,” “Coimbra med.,” 1898, xviii, 87, 88. 7. Chaffee, F. F., “ Chronic Gastritis,” “ Trans. Vermont Med. Soc.,” 1895- ’96; Burlington, 1897, 47-65. 8. Charles, “ On a Case of Cirrhosis, or Fibroid Infiltration of the Stomach,’ “ Dublin Jour, of Med. Science,” 1878. 9. Curschmann, “ Sitzung des Aertzlichen Vereins zu Hamburg vom 19. Mai, 1885,” “ Deutsche Med. Wochenschr.,” 1885. 10. Cutler, E. G., “General Remarks on Gastric Dyspepsia,” “Boston Med. and Surg. Jour.,” 1897, cxxxvil. 11. Deekens, A. H., “Chronic Catarrhal Gastritis: Its Pathology, Sympto- matology, and Treatment,” “Med. Sentinel,” Portland, Oregon, 1898, vi, 123- 134 - 12. Deininger, “ Zwei Falle von Idiopathischer Gastritis Phlegmonosa,” “ Deutsches Archiv fur klin. Med.,” xxiii. 13. Ebstein, “ Ueber die Veranderungen welche die Magenschleimhaut durch Einverleibung von Alcohol und Phosphor erleidet,” “ Virchow’s Arch.,” Bd. lv. LITERATURE ON ACUTE AND CHRONIC GASTRITIS. 479 14. Edinger, “Zur Kenntniss der Driissenzellen des Magens, besonders beim Menschen,” “ M. Schultzer’s Archiv,” Bd. xvii, S. 209. 15. Eisenlohr, “ Ueber primare Atrophie der Magen- und Darmschleimhaut und deren Beziehung zu schwerer Anamie und Riickenmarkserkrankungen,” “ Deutsche med. Wochenschr.,” 1892. 16. Ewald, “ Zur Diagnose und Therapie der Magenkrankheiten,” “ Berlin, klin. Wochenschr.,” 1886. 17. Fenwick, Lecture on “Atrophy of the Stomach,” “ Lancet,” 1877. 18. Fenwick, “On Atrophy of the Stomach,” London, 1880. 19. Fenwick, “ Ueber den Zusammenhang einiger krankhafter Zustande des Magens mit anderen Organerkrankungen,” “Virchow’s Archiv,” Bd. CVIII. 20. Fleiner, “ Erfahrungen iiber die Therapie der Magenkrankheiten,” “ Volkmann’s Sammlung klinischer Vortrage,” Nr. 103, 1894. 21. Fleiner, “Ueber die Behandlung der Constipation, etc., mit grossen Oelklystieren,” “Berlin, klin. Wochenschr.,” 1893, Nr. 3 und 4. 22. Gerhardt, “ Magenkatarrh durch lebende Dipterenlarven,” “ Jenaer med. Zeitschr.,” ill. 23. Glax, “ Die Magenentziindung,” “ Deutsche med. Zeitung,” 1894. 24. Gluzinski, “Ueber das Verhalten des Magensaftes in fieberhaften Krankheiten,” “ Deutsches Archiv f. klin. Med.,” Bd. xlii. 25. Gostkowski, “ Ein Fall von NH 3 Vergiftung mit totaler Abstossung des Magenschleimhaut,” Dissert., Leipzig, i895~’96. 26. Griitzner, P., “ Neue Untersuchungen iiber Bildung und Ausscheidung des Pepsins im Magen,” Breslau, 1875. 27. Hanot et Gombault, “ Etude sur la Gastrite chronique avec sclerose sous- muqueuse hypertrophiqueet retroperitonite calleuse,” “Archiv. de Physiologie,” 1882, IX. 28. Harnack, E., “Ueber die Verschiedenheit gewisser Aetzwirkungen auf lebendes und todtes Magengewebe,” “Berlin, klin. Wochenschr.,” 1892. 29. Hayem, “ Sur l’anatomie pathologique de la gastrite parenchymateuse hyperpeptique,” Paris, 1893. 30. Hayem, “ Classement des varietes anatomiques des gastrites,” “ Soc. Med. des hop. de Paris,” 24, vii, 1896. 31. Hayem, “ Gastrite degenerative,” “ Soc. Med. des hop. de Paris,” 28, x, 1896. 32. Hayem, G., et G. Lion, “ Traitement des gastrites” (Abstr.), “ Rev. de therap, med.-chir.,” Par., 1897, lxiv, 429-433. 33. Henne, “ Experimentelle Beitragezur Therapie der Magenkrankheiten,” “ Deutsche Zeitschr. f. klin. Med.,” xix, Supplement. 34. Honigmann, “ Epikritische Bemerkungen zur Deutung des Salzsaure- befundes im Mageninhalt,” “ Berlin, klin. Wochenschr.,” 1893. 35. Honigmann, “ Ueber einige wesentliche Punkte aus der Diatetik fur Magenkranke,” Sep.-Abdr. aus der “ Zeitschrift fur Krankenpflege,” 1894. 36. Immermann, “Ueber die Functionen des Magens bei Phthisis tuber- culosa,” “ Verhandlungen des Congresses fur innere Medicin,” Wiesbaden, 1889. 37. Jaworski, “ Zur Diagnose des Atrophischen Magenkatarrhs,” “Verhand- lungen des Congresses fur innere Medicin,” Wiesbaden, 1888. 480 CHRONIC GASTRITIS. 38. v. Kahlden, “Ueber chronisch sclerosirende Gastritis,” “ Centralblatt f. klin. Med.,” 1887, Nr. 16. 39. Kalnin, K. K., “ Apropos of Application of Tincture of Iodine in the Treatment of Chronic Gastric Catarrh.” 40. Kaufmann, “ Zwie Falle geheilter pernicioser Anamie,” etc., “Berlin, klin. Wochenschr.,” 1891. 41. King, C., “ Dyspepsia,” “N. Y. Lancet,” 1898, 297-300. 42. Klebs, “ Handbuch d. patholog. Anatomie,” 1868, S. 174. 43. Kiihnau, “Berlin, klin. Wochenschr.,” 1897, No. 19. 44. Kulneff, “Ueber basiche Zersetzungsproducte in Magen- und Darm- inhalt,” “ Berlin, klin. Wochenschr.,” 1891. 45. Kupffer, C., “ Epithel und Driisen des menschl. Magens,” Miinchen, 1883. 46. Leary, F., “Diphtheric Gastritis,” “Jour. Boston Soc. Med. Sc.,” 1897, No. 16, 8-12. 47. Lesser, “ Cirrhosis ventriculi,” Inaug. Diss., Berlin, 1876. 48. Leube, “Ueber die Therapie der Magenkrankheiten,’’ “Volkmann’s Sammlung klin. Vortrage,” 1873, Nr. 62. 49. Leube, “ Beitrage zur Diagnostik der Magenerkrankungen,” “ Deutsches Archiv f. klin. Med.,” 1883, xxxm. 50. Leube, “ Ueber eine neue Art von Fleisch-solution als Nahrungs- und Heilmittel bei Erkrankungen des Magens,” “Berlin, klin. Wochenschr.,” 1873. 51. Litten und Rosengart, “ Ein Fall von fast volligem Erloschen der Secre- tion des Magensaftes (Atrophie der Magenschleimhaut),” “ Zeitschr. f. klin. Med.,” xiv. 52. Losch, “Ueber die nach Einwirkung abnormer Reize auf die Magen- schleimhaut auftretenden pathologisch-anatomischen Veranderungen,” “All- gem. Wien. med. Zeitung,” 1881, Nr. 50. 53. Lyon, G., “ Traitement de la gastrite hyperpeptique ” (Abstr.), “Rev. de therap. med. chir.,” Par., 1898, LXV, 757-766. 54. Marfan, “ Troubles et lesions gastriques dans la phthisie pulmonaire,” Paris, 1889. 55. Manassein, “ Chemische Beitrage zur Fieberlehre,” “Virchow’s Archiv,” Bd. lv. 56. Mathieu, A., “Un cas d’uremie gastrique chronique,” “Bull. gen. d. therap.,” etc., Par., 1898, cxxxvi, 743-750. 57. Mester, B., “Ueber Magensaft und Darmfaulniss,” “Zeitschr. fiir klin. Med.,” xxiv. 58. Meyer, G., “ Zur Kenntniss der sogenannten Magenatrophie,” “ Zeitschr. f. klin. Med.,” Bd. xvi. 59. Mintz, “ Ein Fall von Gastritis phlegmonosa diffusa im Verlaufe eines “ Magenkrebses,” “ Deutsches Archiv f. klin. Med.,” Bd. xlix. 60. Murdoch, F. H., “The Diagnosis and Treatment of Gastric Catarrh,” “N. Y. Med. Jour.,” 1897, lxvii, 289. 61. v. Noorden, “ Ueber die Ausniitzung der Nahrung bei Magenkrank- heiten,” “ Zeitschrift f. klin. Med.,” Bd. xvii. 62. v. Noorden, “ Der Stoffwechsel der Magenkranken und seine anspriiche an die Therapie,” “ Berliner Klinik,” 1893. LITERATURE ON ACUTE AND CHRONIC GASTRITIS. 48 1 63. Nothnagel, “ Cirrhotische Verkleinerung des Magens und Schwund der Labdriisen unter dem klinischen Bilde der perniciosen Anamie,” “Deutsches Archiv f. klin. Med.,” xxiv. 64. Oppler, B., “Der chronische Magenkatarrh und seine Behandlung,” “Berliner Klinik,” 1898, Heft cxxm, 1-25. 65. Oppolzer, “ Erfahrungen iiber die Therapie der Magenkrankheiten,” < ' Zeitschr. d. k. k. Ges. d. Aerzte zu Wien,” Wien, 1857, xm. 66. Penzoldt, “ Beitrag zur Lehre von der menschlichen Magenverdauung,” “ Deutsches Archiv f. klin. Med.,” Bd. Li u. LIU. 67. Penzoldt, “ Salzsaures Orexin, ein echtes Stomachicum,” “ Therapeu- tische Monatshefte,” Februar, 1890. 68. v. Pfungen, “ Ueber Atonie des Magens,” Wien, 1887. 69. Pick (Coblenz), “ Die Behandlung des chronischen Magenkatarrhs mit grossen Bismuthdosen,” “ Berlin, klin. Wochenschr.,” 1893. 70. Popoff, P. M., “ Ueber Magenkatarrh,” “ Zeitschr. f. kl. Med.,” Bd. xxxn, XXII. 71. Quincke, “Luftschlucken,” “ Verhandlungen des VIII. Congresses fur innere Medicin,” Wiesbaden, 1889. 72. Quincke, “ Ueber perniciose Anamie,” “ Volkmann’s Sammlung klin. Vortrage.” 73. Reed, B., “ Diet in the Chronic Catarrh of the Gastrointestinal Tract,” “ Jour, of Am. Med. Assn.,” Feb. 19, 1898. 74. Reichmann, “ Ueber die Anwendung der Pankreaspraparate beim atro- phischen Magenkatarrh,” “ Deutsch. med. Wochenschr.,” 1889. 75. Reichmann, N., “Zur Diagnose der Gastritis atrophicans,” “ Gazetta lekanka (Polnisch) ; “ Berlin, klin. Wochenschr.,” 1898, xxxv, 1015. 76. Riegel, “ Beitrage zur Pathologie und Diagnostik der Magenkrankheiten,” “ Deutsche Archiv f. klin. Med.,” xxxvi ; “ Zeitschr. f. klin. Med.,” xi. 77. Riegel, “Ueber Diagnostik und Therapie der Magenkrankheiten,” “ Volkmann’s Sammlung klin. Vortrage,” 1886, Nr. 289. 78. Rodrigues, d’Oliveira J., “ Nota sobre um caso de gastrite chronica glandular hyperpeptica,” “ Coimbra med.,” 1897, xvii, 458, 474,494. 79. Rosenheim, “ Ueber atrophische Processe an der Magenschleimhaut in ihrer Beziehung zum Carcinom und als selbststandige Erkrankung,” “ Berlin, klin. Wochenschr.,” 1888. 80. Rosenheim, “Ueber die Magendusche,” “ Therapeut. Monatshefte,” 1892. 81. Sachs, “Die Kenntniss der Magenschleimhaut in krankhaften Zu- standen,” “ Archiv fiir exp. Patholog. u. Pharm.,” xxn u. xxiv. 82. Schwalbe, “ Die Gastritis der Phthisiker vom patholog.-anatomischen Standpunkte,” “Virchow’s Archiv,” Bd. cxvii. 83. Senator, “ Ueber ein Fall von Hydrothionanamie und iiber Selbst- infection durch abnorme Verdauungsvorgange,” “Berlin, klin. Wochenschr.,” 1868. 84. Stintzing, “Zur Structur der enkrankten Magenschleimhaut,” “Miinch- ener med. Wochenschr.,” 1889, Nr. 48. 85. Stintzing, “ Miinchener med. Wochenschr.,” 1890. 86. Symes, L., “ Dyspeptic Conditions,” “ Dublin Jour. Med. Sc.,” 1897, civ, 115-121. 482 CHRONIC GASTRITIS. 87. Tawitzki, “ Ueber den Einfluss der Bitterstoffe auf die Mengen der Salz- saure im Magensaft bei gewissen Formen von Magen- und Darmkatarrhen,” “ Deutsches Archivf. klin. Med.,” Bd. xlviii. 88. Tournier, C., “ D’un type de catarrhe gastrique avec hyperesthesie dela muqueuse et colite muco-membraneuse ; difficultes diagnostiques avec l’ulcere,” “ Prov. medicale,” 21, 22, 1897. 89. Uffelmann, “ Beobachtungen und Untersuchungen an einem gastroto- mirten fiebernden Knaben,” “ Deutsches Archiv f. klin. Med.,” xx, 1877. 90. Virchow, R., “ Der Zustand des Magens bei Phosphorvergiftung,” “ Vir- chow’s Archiv,” Bd. xxxi, S. 388. 91. Wasbutzki “Ueber den Einfluss von Magengahrungen auf die Faulniss- vorgange im Darmkanal,’’ “Archiv f. exp. Patholog.,” etc., Bd. xxvi. 92. Werther, “ Ueber den therapeutischen Werth der Pepsinweine,” “ Berlin, klin. Wochenschr.,” 1892. 93. Widal, “ Le Bulletin Medicale,” 1896, Nos. 59, 61, 64, 78, 83, and 1897, No. 4. 94. Will, F. J., “ Gastric Catarrh,” “Trans. Iowa Med. Soc.,” Cedar Rapids, 1897, xv, 299-305. 95. Wolf-Gothenberg, “ Beitrage zur Kenntniss der Einwirkung verschie- dener Genuss und Arzneimittel auf den menschlichen Magensaft,” “ Zeitschr. f. klin. Med.,” Bd. xvi. BIBLIOGRAPHY OF PHLEGMONOUS GASTRITIS. A. 1. Ackermann, “ Ein Fall von phlegmonoser Gastritis mit Thrombose zahl- reicher Magenvenen und embolischen Heerden in der Leber und in den Lungen,” “Virchow’s Archiv,” 1869, Bd. xlv, S. 39. 2. Albers, “ Rheinisch-Westph. med. Correspondenzblatt,” 1884, No. 5, re- ported by “Tillmann’s Archiv f. klin. Chir.,” Berlin, 1882, Bd. xxvil, S. 155. 3. Andral, G., “ Maladies de l’abdomen,” “ Clinique medicale,” 1839, tome 11. 4. Asverus, “Ein Fall von Gastritis phlegmonosa,” “Jenaische Zeitschr. f. med. Natur.,” Jena, 1866, Bd. 11, S. 476-482. 5. Auvray, “ Etude sur la Gastrite phlegmoneuse,” “ These de Paris,” 1866. B. 6. Baerecke, V. Z., “Was it a Case of Phlegmonous Gastritis?” “ N. Y. Med. Record,” 1898, liv. 7. Bamberger, “ Henoch’s Klinik der Unterleibskrankheiten,” Berlin, 1 85 5 ^ Bd. 11, S. 196. 8. Beckler, “Ein Fall von idiopathischer phlegmonoser Gastritis,” “Bayer, Aerztl. Int. Int-Bl.,” Munchen, 1880, Bd. xxvn, Nr. 37, S. 403. 9. Belfrage and Bedenius, “ Schmidt’s Jahrb.,” Leipzig, 1872, Bd. cliv, S. 298. 10. Bianchette, “ Sopra un laso bi Gastrite Flemonosa,” “ Gaz. Med. Ital.,” Prove. Venete. Padova, 1875, vol. xvn, p. 217. 1 1. Bonetes, “ Sepulchretum sive Anatomia Practica,” Lib. ill, Geneva, 1700. 12. Bouveret, “ Traite de pathologia Generale,” 1895, tome 1, p. 781. 13. Bret and Paviot, “ Rev. de med.,” Paris, May 10, 1894, p. 384. 14. Brinton, “ Diseases of the Stomach.” 15. Budd, “ Organic and Functional Diseases of the Stomach,” 1855. LITERATURE ON PHLEGMONOUS GASTRITIS. 483 c. 16. Cahn, “Gastritis diphtheritica mit acuter gelber Leberatrophie,” “ Deutsches Archiv f. klin. Med.,” Leipzig, 1883, Bd. xxxiv, S. 113-121. 17. Callow, vide Auvray ( loc . ci/.). 18. Caudmont, “ Bull. Sec. Anat. de Paris,” 1848, tome xxxm, p. 273. 19. Chvostek, “Zwei Falle von primarer diffuser phlegmonbser Gastritis,” “ Wien. med. Presse,” 1877, Nr. 22, 29, Bd. xvii, S. 693. 20. Chvostek, “ Ein weiterer Beitrag zur primaren diffusen phlegmonosen Gastritis, “ Wien. med. Bl.,” 1881, Nr. 28, Bd. iv, S. 831, 861, 891, 924, 962. 21. Cornil, vide Auvray {loc. cit., p. 20). 22. Cruveilhier, vide Raynaud, p. 526. D. 23. Deininger, “Zwei Falle von idiopathischer Gastritis phlegmonosa,” “ Deutsches Archiv f. klin. Med.,” Leipzig, 1 878— ’79, Bd. xxn, S. 624-632. 24. Dirner, “Gastritis phlegmonosa,” “ Orbosi hetila,” Budapest, 1881, vol. xxv, page 793. 25. Dumesnil, vide Auvray {loc. ci/.). E. 26. Ewald, “Lectures on Diseases of the Stomach,” “ N. Sydenham Soc. Trans.,” 1892, p. 504. (Cases reported from clinic of Frerichs.) 27. Fagge, “ A Case of Diffused Suppurative Inflammation of the Stomach,” “ Trans. Path. Soc.,” London, 1874-75, vol. xxvi, p. 81. 28. Feroci, “ Ann. univ. di med. e chir.,” Milano, 1873. 29. Ferraresi, “ Sulla Gastrite Flemmonoso,” “ Atti Accad. med. di Roma,” 1887, series xi, vol. cxi, p. 267. 30. Flint, quoted by Reinking {loc. cit.), S. 16, “ Phila. Med. Times,” Aug. 8, 1878. 31. Fontain, “ Gastrite Phlegmoneuse,” “ Bull, et mem. Soc. med. d. hop. de Paris,” 1866, tome xi, p. 131. 32. Frankel, “ Ueber einen Fall von Gastritis acuta emphysematosa, wahrscheinlich mykotischen Ursprungs,” “Virchow’s Archiv,” 1889, Bd. cxviil, S. 526. G. 34. Garel, cited by Reinking, 1879 {loc. cit.), S. 17, “ Lyon med.,” Oct., 1871. 35. Gaudy, “Observation de Gastrite Phlegmoneuse,” “Archiv Med. Beige,” Bruxelles, 1863, tome xxxi, pp. 459-464. 36. Gilbert and Dominici, “ Med. Jour.,” New York, May, 1894; cited from Leith’s article {loc. cit.). 37. Glaser, “ Zwei Falle von Gastritis phlegmonosa idiopathica,” “ Berl. klin. Wochenschr.,” 1883, Bd. xx, S. 790. (Two cases.) 38. Glax, “Ueber Gastritis phlegmonosa,” “ Berl. klin. Wochenschr.,” 1879, Bd. xvi, S. 565. 39. Glax, “Die Magenentziindung,” “Deutsche med. Ztg.,” Beilin, 1884, Nr. 3. 40. Guyot, “Gastrite Phlegmoneuse,” “Union med.,” Paris, 1865, N. S., tome xxvii, pp. 184, 185. 484 CHRONIC GASTRITIS. H. 41 (a). Habershon, “ Case of Suppuration in the Coats of the Stomach,” *' Guy’s Hosp. Rep.,” London, 1855, p. 1 1 5. 41 ( b ). Hemmeter, John C. “ A case of phlegmonous Gastritis,” etc., “New York Med. Rec.,” Sept., 1897. 42. Herzog, “ Kaspar’s Wochenschr.,” 1839, S. 813; quoted by Reinking {loc. cit ., S. 11). 43. Heyfelder, “ Sanitatsbericht liber das Fiirstenthum Hohenzollern Sig- maringen wahrend des Jahres 1836,” “ Schmidt’s Jahrb.,” Leipzig, 1837, Bd. xvi, S. 192. 44. Hun, “Idiopathic Phlegmonous Inflammation of the Submucous Cellu- lar Tissue of the Stomach,” “ N. Y. Med. Jour.,” 1868, vol. vm, p. 18. 45. Kelynack, “A Case of Diffuse Phlegmonous Gastritis,” “Lancet,” London, 1896, March 14th. 46. Klaus, “ Beitrag zur Kenntniss d. Magenkrankheiten,” Inaug.-Diss., Erlangen, 1857. 47. Klebs, “ Ueber infectiose Magenaffectionen,” “ Allg. Wien. med. Ztg.,” 1881, Nos. 29, 30, 31, 32, 34, 35. 48. Krabbe, “ Tidsker. f. Vet.,” Kjobenhaven, 1872; and “Deutsche Zeitschr. f. Thiermedicin,” Leipzig, Bd. 1. 49. Krause, “Ueber submucose phlegmonose eitrige Magenentziindungen,’ Berlin, 1872, Inaug.-Diss., Kiel, 1874. 50. Kurschmann, “ Magenabscess,” “Wien. med. Wochenschr.,” 1880, No. 14. L. 51. Lasege, vide Auvray {loc. cit.). 52. Leith, “Phlegmonous Gastritis: Its Pathology, Etiology, Symptoms, and Treatment,” “Edinburgh Hospital Reports,” vol. iv, pp. 51-114. 53. Leube, “ Ziemssen’s Cyclopaedia of the Practice of Medicine,” 1877, vol. vii, p. 154. 54. Lewandowski, “Zur Casuistik der idiopathischen Gastritis phlegmo- nosa,” “ Berlin, klin. Wochenschr.,” 1879, Bd. xvi, S. 568. 55. Lewin, “ Zur Casuistik der Gastritis phlegmonosa idiopathica,” “ Berlin, klin. Wochenschr.,” 1884, Bd. XXI, S. 83. 56. Lieutaud, “ Historia Anatomica-medica ” (includes observations by Riolanus, Baunimus, and others), 1767, tome 1, p. 2. 57. Lindemann, “ Fall von Gastritis phlegmonosa diffusa,” “ Munch, med. Wochenschr.,” 1887, Nr. 25. 58. Lowenstein, “Ueber Gastritis phlegmonosa,” Inaug.-Diss., Kiel, 1874. 59. Loomis, “Med. Rec.,” N. Y., Feb. 15, 1869. M. 60. Macleod, “Suppurative Gastritis,” “ Lancet,” London, 1887, vol. xi, p. 1116. 61. Malmsten and Key, “ Fall af Flegmonos Gastritis, Hygeia,” Stockholm, 1871, p. 69. 62. Manoury, “Infiltration Purulente Puerperale de l’Estomac,” “Bull. Soc. Anat. de Paris,” 1842, tome xvii, p. 175. LITERATURE ON PHLEGMONOUS GASTRITIS. 485 63. Martin, “ Diseases of the Stomach,” 1895, p. 277. 64. Mascaral, “Bull. Soc. Anat. cle Paris,” 1830, tome xv, p. 176. 65. Mayor, “ Absces Sous-muquex de l’Estomac,” “Bull. Soc. Anat. de Paris,” 1840, tome xvn, p. 298. 66. Mazet, “Phlegmon. Diffuse de l'Estomac,’’ “ Bull. Soc. Anat. de Paris,” 1840, tome xv, p. 174. 67. Meyer, “St. Petersb. med. Wochenschr.,” 1892, No. 40. 68. Mintz, “ Ein Fall von Gastritis phlegmonosa diffusa im Verlaufe eines Magenkrebses,” “ Deutsches Archiv f. klin. Med.,” Leipzig, 1892, Bd. xlix, S. 487. 69. Morel, “ Gastrite Phlegmoneuse,” “ Bull. Soc. Anat. de Paris,” 1865. N. 70. Nasse and Orth, “Virchow’s Archiv,” Bd. civ, S. 584. 71. Nielsen, “ Bradsot hos Faaret (Gastromycosis ovis),” “ Tidsker. f. Vet.,” Kjobenhaven, 1887, pp. 1-2 1. O. 72. Odmanson, “Gastritis phlegmonosa diffusa,” “ Forh. v. Svens Lak. Sallsk. Sammank,” Stockholm, 1865, p. 265. 73. Oser, “ Realencyclopadie ” : “ Magenentziindung,” 1887, Bd. xi, S. 412. P. 74. Page, “A Case of Gastrostomy Fatal on the Twenty-third Day, from Acute Parenchymatous Gastritis,” “Lancet,” London, 1833, vol. 11, p. 53. 75. Petersen, “Ein Fall von Gastritis phlegmonosa,” “St. Petersb. med. Wochenschr.,” 1879, Bd. iv, S. 288. 76. Pilliet, “ Bull. Soc. Anat. de Paris, 1893, No. 12. 77. Rakowak, “ Duchek’s Klinik; “Wien. med. Presse,” 1873, No. 25. 78. Raynaud, “ De l’lnfiltration Purulence de l’Estomac,” “ Bull. Soc. Anat. de Paris,” 1861, tome vi, pp. 62-93. 79. Reinking, “ Beitrag zur Kenntniss der phlegmonosen Gastritis,” Inaug.- Diss., Kiel, 1890, S. 26. 80. Robel, P., Opera, 1656. S. 81. Sand, “ Dissertatio de raro Ventriculi Abscessu Regiomont,” 1701. 82. Sebillon, “ De la Gastrite phlegmonosa,” “These de Paris,” 1885. 83. Sestier, “ Abscess Metastatique des Parois de l’Estomac,” “Bull. Soc. Anat. de Paris,” 1883, tome vm, p. 130. 84. Silcock, “ Stomach Exhibiting the Condition known as Phlegmonous Gastritis,” “ Trans. Path. Soc.,” London, i882-’83, vol. xxxiv, p. 90. 85. Smirnow, “ Ueber Gastritis membranacea und diphtheritica,” “ Virchow’s Archiv,” 1889, Bd. cxm, S. 333. 86. Smith, “ Med. Rec.,” New York, Oct. 12, 1889. 87. Stewart, “A Case of Gastritis Phlegmonosa, with Inflammation and Gangrene of the Gall-bladder,” “ Edin. Med. Jour.,” 1868, N. S., vol. xn, P- 732 . 88. Strieker und Kooslakoff, “ Experimente iiber Entziindungen des Magens," “ Sitzungsb. d. k. Akad. d. Wissensch.,” Wien, 1866, Bd. liii. 32 486 ULCER OF THE STOMACH. T. 89. Testi, Alberico, “Un raro caso di ascesso dello stomaco,” “ Annal univ. di med. e chir.,” Milano, Dec., 1883, pp. 523-547. 90. Thoman, “Allgem. Wiener Zeitung,” 1891, Nr. 10. 91. Thungel, “ Ein Fall von Vereiterung des submucosen Zellgewebes des Magens,” “ Virchow’s Archiv,” 1865, Bd. xxxm, S. 406-408. 92. Treuberg, “Primary Phlegmonous Inflammation of the Stomach,” “ Vrach,” St. Petersb., 1883, vol. lv, p. 355. 93. Varandaeus, “ Tractatus de Morbis Ventriculi,” 1620. 94. Vorwaltner, “ Eph. Nat. cur.,” Dec. 3, Obs. 142. 95. Wallmann, “Wiener med. Wochenschr.,” 1857, Bd. xm, S. 733. 96. Whipham, “ Remarks on a Case of Phlegmonous Gastritis,” “ Brit. Med. Jour.,” London, 1884, vol. 1, p. 896. 97. Wilks and Mokon, “ Pathological Anatomy,” 3d edition, 1889, p. 399. 98. Ziegler, “ Pathologische Anatomie,” Bd. 11, S. 513. CHAPTER III. ULCER OF THE STOMACH. Ulcus Ventriculi , Pepticum , Rotundum , Perforans , Rodens , Corrosivum , e Digestione. Ulcer of the stomach is a loss of substance of the gastric mucosa, characterized by very little tendency toward healing, but rather by destructive progression both in a lateral direction — i. e. y in a plane with the surface — and toward 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 peri- toneum, with such small lateral involvement, that Rokitansky’s original comparison, “ as 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 terraced 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 SELF-DIGESTION OF THE STOMACH. 487 causes cicatricial contractions and deformity. The acute form may terminate in healing, but owing to its limited lateral extent, the small cicatrix rarely causes deformity. It is very probable that the acute ulcers have a different etiology (corrosives, toxic action, trauma by sharp, hard materials in the food, in conjunction with other factors to be considered) from the chronic eroding type, to which the following description appertains more especially. Self-digestion of the Stomach (Gastromalacia). — If an animal be killed while in full digestion, the stomach may undergo self- digestion after death if the body is kept warm. In human beings who died suddenly while the gastric digestion was at its hei'ght, it was found at the autopsy that not only the stomach had been digested, but also the spleen, and that this process had extended through the diaphragm into the lungs. The question naturally arises, What protects the stomach from autodigestion from its own secretions under normal conditions ? This is an inquiry that con- cerns the fundamental properties of living matter, for it includes the non-digestion of the intestinal tract by the alkaline pancreatic juice and succus entericus, the same property as observed in the digestive tracts of invertebrates and even in the unicellular organ- isms, the amebae and plasmodia of mycetozoa. For instance, Metschnikofif, C. Le Dantec, Greenwood, Saunders, and the author have shown that a secretion is formed in the digestive vacuoles of these unicellular organisms which digests foreign 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, Philos. D., etc., in “American Naturalist,” August, 1896, p. 619). The following explanations have been offered for the protection of the human stomach from its own secretion : 1. By Hunter: That the principle of life in living things pro- tected the stomach from digestion. Bernard succeeded in demonstrating that the hind leg of a living frog, introduced into a dog’s stomach through a fistula, under- goes digestion. This will also happen if the leg be placed in a vessel containing gastric juice at the proper temperature. 2. Bernard explained the exemption of the normal stomach from autodigestion by assuming a protective power in the living epithelium, which he thought prevented the absorption of gastric juice. 3. Strieker believed that the mucus formed on the surface of the stomach acts as a protective covering. 488 ULCER OF THE STOMACH. 4. Pavy (“Guy’s Hospital Reports,” vol. xiv, 1868) held that the alkaline blood circulating through the gastric walls saved them from digestion, since it neutralized the acid as fast as it was ab- sorbed. None of these explanations is sufficient. Bernard’s sug- gestion simply shifts the problem by assuming an immunity of the living epithelial cells without attempting to explain why these are not digested. The coating of mucus which Strieker believed to be a protection is digested by gastric juice. Pavy’s theory that the alkaline reaction of the gastric circulation prohibits self-digestion, is untenable, because under these condi- tions one could not explain why the pancreas does not digest itself, and is also disproved by Samelson, who produced a neutral reac- tion of the blood by gradual introduction of acid, and then poured dilute HC 1 into the animals’ stomachs; but even then no auto- digestion was observed. When Hunter, over one hundred years ago (1786), referred the immunity to a specific property of the living cells, the “ vital principle,” he gave as good an explanation as any given up to date. The expression “ vital principle ” may sound mysterious in the light of modern physiological knowledge, but it undoubtedly implied that gastric immunity from self-diges- tion was due to physical and chemical forces possessed by the protoplasm of living cells and which are not as yet understood. In the latter term we use more accurate expressions, but give no better explanation than Hunter. Elsasser agreed that gastromalacia was always a cadaverous process, and was supported in this view by Virchow, Foster, Oppolzer, Bamberger, and others, so that his opinion became the prevailing one. A contrary view was held by Rokitansky, who represents the belief that there is a gastromalacia that occurs intra vitam } particularly in the end stages of grave diseases of the brain and its membranes (basal and tuberculous meningitis) and in other severe exhausting affections. The occurrence of intravital autodi- gestion was proved in a case reported both by W. Mayer and Leube from Ziemssen’s clinic, and also by numerous animal experiments. Results of animal experiments in producing secondary injury and consequent self-digestion of the stomach are the following : Schiff, by intersection of the thalami and cerebral peduncles, pro- duced hemorrhagic infiltrations, partial softenings, erosions, and even ulcer formation in the gastric mucosa, and interpreted his results as consequences of neuroparalytic hyperemia caused by injury to the central vasomotor nerve- tracks of the stomach. EXPERIMENTS BEARING ON THE ETIOLOGY. 489 Ebstein and Brown-Sequard obtained identical effects after circum- scribed destruction of the anterior corpora quadrigemina. Panum injected an emulsion of tiny wax globules into the femoral arteries of dogs and effected small gastric hemorrhagic infarcts and ulcers. Cohnheim injected suspensions of plumbic chromate into the stomach circulation, by which he succeeded in blocking only the branches of the mucosa and submucosa, while the circulation of the muscularis remained free. At the autopsy he discovered large ulcers with abruptly descending edges and clean bases. Koch and Ewald brought about gastric hemorrhagic infarcts by intersection of the spinal cord (Schiff’s method), and after this introduced strong solutions of hydrochloric acid (5 per 1000) into the stomach, thereby producing penetrating ulcerations. After severe traumatism, — for example, bruising the epigastric region with a hammer, — and after thermic irritation, as by introducing very hot gruel, Ritter and Decker produced ulcus ventriculi. Silbermann brought on gastric ulcers that healed with difficulty by causing hemoglobinemia with substances that dissolved the blood-cor- puscles. His results are significant, as explaining the pathogenesis of gas- tric ulcer after extended skin burns and malaria. This is to a certain entent explained by the investigations of Klebs and Welti, who have shown that broken-down red corpuscles, blood-pigment and thrombi of blood-plaques, or undeveloped elements may occlude the gastric vessels and cause ulcer; and London explains the gastric ulcers in malaria by the occurrence of pigment emboli. Talma produced gastromalacia and gastric ulcers by ligating the esophagus of dogs above the cardia and the duodenum below the pylorus (Talma, “ Untersuch. fiber Ulcus ventric,” etc., “ Zeitschr. f. klin. Med.,” Bd. xvii, S. 10). This experiment constitutes too vio- lent an interference with normal gastric physiology to permit of any correct deductions. It is impossible to differentiate the effects of violent trauma, inter- ference with the venous, arterial, and lymph-supply, intragastric stagnation, fermentation, and sepsis, that the experiment of Talma brings about. Views Concerning Causative Circulatory Disturbances. — Virchow called attention to the frequency of gastric ulcers in anemia and chlorosis, explaining it by the diseases of the vessel walls, fatty degenerations, aneurysmal and varicose dilatations, and their consequences, viz. : thrombosis and embolism. Cohnheim 490 ULCER OF THE STOMACH. conceded the casual relations of these states, but disputed the fre- quency of their occurrence, (i) because the abundant anastomoses between the gastric vessels facilitate a compensatory collateral cir- culation ; ( 2 ) because the diseases of the vessel walls referred to are rare in young, but frequent in old persons, which would indi- cate that in these, gastric ulcer should be found frequently, whereas in later life it is very rare. Klebs has a theory attributing gastric ulcer to local ischemia, supposed to be caused by spastic arterial contractions. Rindfleisch’s opinion is that venous stasis in the gas- tric walls may lead to ulcer, since occlusion of the exit of the blood may occur easily on account of the compressibility and the few anas- tomoses in the gastric veins ; this, he thinks, may cause hemorrhage, erosions, and ulcer. Cohnheim opposes this view also, because gastric ulcer is a rare thing in the passive congestion due to hepatic cirrhosis. One must not overlook the fact, however, that in this state the secretion of HC1 is much reduced. Axel Key assumes that long and persisting contractions of the musculature may cause local ischemias or disturbances in the venous outflow. From these observations it is clear that interruption of the blood-current in localized areas of the mucosa may lead to formation of ulcer. The blood stream, then, is a protective against autodigestion, not because it keeps the gastric mucosa alkaline, as Pavy held, — for the mucosa is acid throughout the glandular layer, — but because the blood keeps the mucosa nourished and alive. When the internal surface of the stomach is no longer nour- ished, it must die in areas, which are then digested, as other dead proteid matter would be. The degree of alkalinity of the human blood is far too low to neutralize the degree of HC1 acidity present in any part of the mucosa. The digestion of the hind leg of a live frog (Bernard) in the stomach of an animal does not prove that living tissue will be digested there. For the cells of cold-blooded animals die rapidly at the temperature of the warm-blooded animal ; furthermore, the epi- dermis of the frog’s leg may be killed by the HC1, and once dead, it is rapidly digested. Bottcher and Letulle attribute the causation of ulcer to bacteria, which they could demonstrate in colonies in the floor and in the surroundings of ulcer. Most of the observers mentioned make the statement that gastric ulcers produced experimentally in animals heal rapidly. The Edge of the Sphincter nomatous ulcer. of the pylorus. PLATE VII ETIOLOGY OF PEPTIC ULCER. 49 1 mucosa is replaced almost completely; a new formation of peptic glands has been observed by Grifinni, Hauser, and Vassali. At autopsies, cicatrices are often found in the human stomach, where no symptoms referable to ulcer were evident during life. It is known, also, that pieces have been torn loose by the suction of the lower end of the stomach-tube, and yet this loss of substance healed without forming an ulcer; so that repair may follow injury to the human stomach, and it is very evident that some other causatory factors besides injury are necessary to bring about an ulcer. A pathological composition of the blood has been thought to be one of these factors, particularly as gastric ulcer is very fre- quently found in anemia and chlorosis. I have analyzed the gastric contents of 32 cases of chlorosis — of these, 24 had marked hyper- acidity ; in 6 the acidity was normal and in 2 it was subnormal. This frequent coexistence of hyperacidity with chlorosis has been observed by Riegel, Cantu, and Bouveret, and is important for the etiology. This view is supported by the experiments of Quinke and Daettwyler, who produced a high degree of anemia by gradual withdrawal of blood from dogs. Thereafter, they produced gastric injuries by mechanical, chemical, and thermic irritants, and discov- ered that ulcers were formed that healed with much difficulty. Clinical experience confirms these observations, that an impaired state of the blood may greatly protract healing. On the other hand, there are numerous records of severe and recurrent attacks of gastric ulcer in persons whose blood was found perfectly normal. Etiology. — The deductions from the preceding summary of experiments and observations are, above all, the establishing of four principal factors in the etiology of ulcer: I. An impaired vitality or resistance of portions of the mucosa. II. Hyperacidity or supersecretion. III. An altered state of the blood. IV. Local bacterial infection. There are a number of well-authenticated cases on record prov- ing that direct trauma may cause gastric ulcer (vide Einhorn, loc . cit., p. 191 ; also others reported by C. Hoffmann, Leube, and Eichhorst). According to Sidney Martin (loc. cit., p. 410), there are three common causes of the death of the tissue which precedes ulceration : I. Mechanical and Chemical Causes . — Ingested fish-bones, egg and oyster shells, seeds, etc. Corrosive poisons lead to ulceration 49 2 ULCER OF THE STOMACH. by directly destroying the tissue; and an injury to the mucous membrane, which is subsequently exposed to the continued action of an irritant, will also lead to an ulcer. Direct injury and wounding of the gastric mucosa occurs very frequently, and, as a rule, heals very rapidly. There are a number of cases on record of persons swallowing glass, nails, and knives, which passed through the entire intestine without causing injury. Marcet (“ Med. Chirur. Transactions,” vol. xn, p. 72) narrates the case of an American sailor swallowing some thirty pieces of knife- blades, which were found in his stomach, together with a number of handles. Two blades were in the colon and rectum, placed transversely, and had perforated the intestinal wall without causing peritonitis. No recent or old ulcers were found in the stomach. The following report from the German Hospital, of Kansas City, goes to show that this class of human ostrich has not died out. The main fact that is proved by such cases is that something else is needed in addition to direct injury to the stomach in order to produce an ulcer. German Hospital, Kansas City, Mo., June 14, 1897. — Harry Whallen, the “human ostrich,” who was operated upon at the German Hospital last Satur- day, and from whose stomach the surgeon took an assortment of cutlery and hardware, died at two o’clock this morning, the result of the operation. Whallen got into trouble by swallowing a big Barlow knife, in Pilot Grove, Mo. When he was operated upon at the German Hospital these articles were removed from his stomach : Two jack-knives, one 3 inches long and the other 4 inches ; 5 knife-blades, from 1 to 3 inches long ; 32 wire nails, eightpenny or larger ; 34 sixpenny nails, 26 shingle nails, 16 carpet tacks and small wire nails, 1 barbed wire staple, 1 horseshoe nail, 3 screws, 3 ounces of glass, and several bits of crockery. He was a professional showman. He began swallowing glass and nails when he was ten years old, and says he has eaten a lamp chimney nearly every day during the seventeen years he has been at it, but the Barlow knife, which he swallowed last week, was too much, even for his long-suffering stomach. When the surgeons operated upon him, the stock of hardware inventoried was found imbedded in a solid mass in his stomach and partially encysted. After it was removed, the stomach was thoroughly washed out and sewed up. 2. 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 means of thrombosis or embolism. Thrombosis takes place in connection with disease of the vessels and in association with inferior quality BACTERIAL INFECTION. 493 of the blood and a slowing of the local circulation ; embolism may be infective or non-infective, and is usually capillary. 3 . Bacterial Infection . — The infective processes of the digestive mucosa with which we are most familiar are the ulceration pro- cesses of typhoid fever, certain dysenteries, and tuberculosis. In the gastric ulcer, however, there is another kind of bacterial infec- tion, which is not accompanied with the signs of active inflam- mation, 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 HC1 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, or very little, HC1 is secreted. There is room for the suggestion that the primary necrosis is due to bacteria and the ensuing ulceration caused by the action of the gastric juice. The bacteria can exist in the cells around and beneath the floor of the ulcer, and 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, while the floor of the ulcer was in the muscularis. It is conceivable that they pave the way for autodigestion by causing necrosis 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 re- sembling that of anthrax, and in two cases of ulcus carcinomatosum the Oppler-Boas bacillus. Thermic causes are the ingestion of very hot food and drink, taken when the organ is empty. An interesting etiological relation exists between cutaneous burns and gastric or duodenal ulcers. The last two factors, hot food and large cutaneous burns, are given in explanation of the reported frequency of gastric ulcer among cooks, who are in the habit of tasting foods that are still on the fire, and who are also liable to frequent burns. However, there is no satisfactory statistical evidence that gastric ulcer is more frequently diagnosed in cooks than in other trades. Constitutional causes are generally brought about by such dis- eases as effect alterations and degeneration either in the com- position of the blood or in the vessels. These are chlorosis, 494 ULCER OF THE STOMACH. anemia, syphilis, tuberculosis, arteriosclerosis ; fatty, amyloid, and aneurysmal degenerations of arteries ; thrombi, emboli, trichinosis, and malaria. Effect of pressure exerted upon the stomach by the costal mar- gins is claimed to induce anemia and atrophy of the mucosa, especially in the region of the smaller curvature. Habershon and Rasmussen have advanced this view, in explanation of the fre- quency of gastric ulcer in those whose occupations necessitate continual pressure on the stomach. Influence of Age . — In order to determine from postmortem records the age at which gastric ulcer most frequently occurs, all cases in which only cicatrices are found should be excluded, because a cicatrix gives no evidence as to the age at which the ulcer existed. The best statistics on this subject are contained in Welch’s article on Gastric Ulcer in Pepper’s “ System of Medicine,” volume ii, page 483. The statistics of Brinton, which are still cited in the last editions of Boas, Fleischer, Sidney Martin, Fleiner, Debove and Remond, and others, include all cicatrices found at autopsies as open ulcers. The following table is given by Welch, representing the age in 607 cases of open ulcer, collected from hospital statistics : Age, . [-10 10-20 20-30 30-40 40-50 50-60 0 r-^ O 70-80 80-90 90-100 Over 100 No. of Cases, - 32 119 107 114 108 84 35 6 0 * Totals, 33 226 222 II 9 7 From this table it is apparent that the largest number of cases is found between twenty and thirty. Three-fourths of the cases occur between twenty and sixty. In 41,688 cases, constituting the clinical material in Zurich and Breslau between the years 1853 an d 1 873, 252 cases of gastric ulcer were diagnosed during life by Lebert; nearly seven-tenths were between twenty and forty years of age, — a preponderance sufficiently great to be of diagnostic value in the differentiation, as we shall see later from carcinoma, for in this disease the largest number of cases is found between fifty and sixty years. Goodhart has described a case of gastric ulcer in an infant thirty hours old. THE FREQUENCY OF GASTRIC ULCER. 495 Influences of Sex . — Females are more frequently affected than males; the following are the figures given by various authors: Males. Females. Welch, 40 per cent. 60 per cent, in 1699 cases of gastric ulcer found at autopsy. Brinton’s ratio, . . 1 male to every 2 females. Anderson, .... 3 males and 32 females in 35 cases. Habershon, ... 74 males and 127 females in 201 cases. Steiner’s ratio, . . 8 males to 1 1 females. The nursing period, puerperium, and menstruation are, it is claimed, liable to increase the susceptibility to ulcer. Geographical Distribution . — There seems to be an unequal geo- graphical distribution of the disease, which seems to be more coVnmon in northern than in southern countries. It is less com- mon in this country than in England and Germany, according to Da Costa, Keating, and Welch ( loc . cit ., p. 485). The last-men- tioned author found only six cases of gastric ulcer in 800 autopsies made by him in New York. In 444,564 deaths in New York City, from 1868 to 1882, ulcer of the stomach was assigned as the cause in only 410 cases. To these statistics little importance can be attached, because they are compiled from reports of practitioners of varying diagnostic skill, and concern a disease that presents many difficulties of recognition. The Frequency of Gastric Ulcer. — We quote the following from Professor Welch’s article {loc. cit .) : In 32,052 autopsies made in Prague, Berlin, Dresden, Erlangen, and Kiel, there were found 1522 cases of open ulcer or of cicatrix in the stomach. If all the scars be reckoned as healed ulcers, according to these statistics gastric ulcer, either cicatrized or open, is found in about five per cent, of persons dying from all causes. It is important to note the relative frequency of open ulcers as compared with that of cicatrices. In 11,888 bodies examined in Prague, there were found 164, or 1.4 per cent., with open ulcers, and 373, or 3.1 per cent., with cicatrices. Here scars were found about two and one-fourth times as frequently as open ulcers. The observations of Grunfeld in Copenhagen show that when especial attention is given to searching for cicatrices in the stomach, they are found much more frequently than the figures here given would indicate. It would be a moderate estimate to place the ratio of cicatrices to open ulcers at three to one. The statistics concerning the average frequency of open ulcers 49 6 ULCER OF THE STOMACH. are much more exact and trustworthy than those relating to cica- trices. It may be considered reasonably certain that, at least in Europe, open gastric ulcers are found, on the average, in from one to two per cent, of persons dying from all causes. It is manifestly impossible to form an accurate estimate of the frequency of gastric ulcer from the number of cases diagnosed as such during life, because the diagnosis is in many cases uncertain. Hence the importance of autopsy statistics. Von Jaksch (cited by Bamberger, “ Handbuch d. speciel. Path u. Therap.,” von Virchow, vi, i. Abth., 280) states that 1 13 ulcers or cicatrices were found in 2330 autopsies, i. e. y 4.8 per cent. Orth gives five per cent. Berthold’s statistics from the “ Charite,” Berlin, from 1868 to 1882, give 294 cases, — 2.7 per cent. (“ Statist. Beitrage z. Kennt. d. chronischen Magengeschwiirs,” Sections-Protocoll d. Path. Inst., Berlin). Nolte, Munchen, 1876 to 1883, gives 3500 autopsies, with 43 ulcers, or 1.23 per cent. (“ Haufigkeit d. Magengeschwiirs in Munchen,” Dissert., 1883). Berthold (cited from Ewald, “ Diseases of the Stomach,” p. 233) gives the percentage of ulcer of the stomach for Berlin as 2.7 per cent.; Nolte, for Munich, as 1.23; Gries, for Kiel, as 8.3; Stark, for Copenhagen, as 13 per cent. Von Sohlern (“ Der Einfluss der Ernahrung auf die Entstehung des Magengeschwiirs,” “ Berlin, klin. Wochenschr.,” 1889, No. 14) has lately called attention to the fact that the Roen Mountains and the Bavarian Alps (Germany) and the greater part of Russia are nearly exempt from gastric ulcer. The diet upon which the inhabitants of these countries subsist consists largely of amylaceous and vegetable substances containing a large percentage of potassium salts. The blood of persons living largely or exclusively on a vegetarian diet (Japanese) is very rich in potassium phosphate. According to von Sohlern, the exemption from gastric ulcer observed among these peoples is due to the large amount of potassium introduced in their food. We are not aware that von Sohlern has supported his theory by quantitative blood analyses ; this constitutes a weak point in his argument. Location of Gastric Ulcer. — This table gives the situation of 793 ulcers reported in hospital statistics (from article on “ Simple Ulcer of the Stomach,” by W. H. Welch, M.D., Pepper’s “ System of Medicine,” vol. 11) : SYM PTO MATO LOGY. 497 Lesser curvature, 288 (36.3 per cent.) Posterior wall, 235 (29.6 “ “ ) Pylorus, 95 ( 12 “ “ ) Anterior wall, 69 ( 8.7 “ “ ) Cardia, 50 ( 6.3 “ “ ) Fundus, 29 ( 3.7 “ “ ) Greater curvature, 27 ( 3.4 “ “ ) Symptomatology. — The most characteristic subjective signs of gastric ulcer are localized pain, vomiting, hematemesis, disturb- ances of secretion, the presence of blood in the stools, and the state of the appetite. Frequently all these symptoms occur together; at other times only one or the other single symptom becomes prominent. There are cases of gastric ulcer that run a latent course, without any characteristic symptoms whatever. We will begin with a consideration of the excessive secretion of HC 1 . This is a result of the irritation of the gastric nerves, either by the inflammation caused by the ulcer itself, or by irritation of exposed nerve-fibers, caused by the contents of the stomach. Since the publication of the first edition of this work, Prof. J. P. Pawlow has demonstrated the secretory nerves of the stomach in the vagus and sympathetic by methods irreproachable from the standpoint of physiological technique. By admirable patience he succeeded in preparing such vagus fibers as caused only a prompt secretion of gastric juice and others that responded to stimulation by prompt inhibition of secretion (Pawlow, “ Arbeit d. Verdauungsdriisen,” S. 78). Just as the eye will overflow with tears until an offending foreign body has been removed, and just as the saliva will be secreted when the mucous membrane of the mouth is stimulated by food, or when there are ulcers or inflammations present in the buccal cavity, so in a similar manner the gastric mucosa will re- spond to irritation of its nerve-fibers by an augmented secretion. The entire gastric nerve apparatus is placed in a state of increased excitability through the presence of an ulcer, and when food reaches the stomach the mucosa is stimulated to a degree much greater than in the normal stomach. The percentage of HC 1 present varies from three to five per 1000; this strong gastric juice rapidly dissolves albuminous constituents of the food, while the carbohydrates remain undigested. Organic acids are absent. It may happen, in rare cases, that the peristalsis of the stomach is in- hibited, causing retention of the food ; in such cases the irritation of the nerves is kept up as long as food is present in the stomach, 498 ULCER OF THE STOMACH. constituting continued hypersecretion. We have to distinguish in these cases between two kinds of excess of gastric juice: (i) the digestive hyperacidity , which occurs when the motility is good, only during the normal presence of ingesta in the stomach ; ( 2 ) the con- tinued hypersecretion , which occurs as soon as the motility is im- paired, when food is present at all times in the organ. With a continued hypersecretion the glandular cells gradually become exhausted; they eventually secrete a juice which is much poorer in HC1 and pepsin than the normal product, just as the exhausted salivary gland-cells secrete a saliva which is very poor in ptyalin. The exhaustion of the gastric gland-cells may explain the observa- tion referred to, where hyperacidity was absent in cases of un- doubted gastric ulcer. The fact probably was, the glands had become so exhausted by continued overwork that it was impossi- ble for them to form their characteristic product. The pain of gastric ulcer is caused by irritation of the sensory nerves in the base of the corroded area. It occurs with great in- tensity after the ingestion of food, and, as a rule, increases with the augmentation of acid during digestion. The pain during the digestive act is most probably caused also by the peristaltic move- ments, drawing upon and compressing the ulcer. External pres- sure will produce sharp pain in the locality of the ulcer. The pain is of a burning, stinging character, and in some cases it causes a spastic contraction of the sphincter of the pylorus re- flexly — a reflex pylorospasm, which in itself may be very painful. Some patients complain frequently of a sore spot in the epigas- trium. In cases of gastric ulcer associated with pylorospasm the pain radiates from the epigastrium toward the right and left, reach- ing the spinal column. Traube called attention to well-defined irradiations of the pain into the domain of other nerves outside of the stomach. Attacks of angina pectoris, intercostal neuralgias, and neuralgias in the left brachial plexus have been described by Brinton ; sympathetic neuralgias in the arms and legs have been referred to by M. Muller. The intercostal nerves of the left side may be in a more sensi- tive condition earlier than those of the right side. This may reveal itself by a hyperesthesia of the skin and soft parts in the lower left parts of the thorax, upper portions of the abdomen, and in the lumbar region. The slightest touch, the pressure of the clothes and bed-covers, may be unpleasant to such patients. Female patients can not wear a corset. PYROSIS. 499 Very frequently the pain has a penetrating, lancinating char- acter, shooting from the epigastrium straight through to the spinal column. The influence of the ingestion of food on the pain is very evident, although there are painful sensations when the stomach is empty; these sensations partake more of the nature of soreness and hunger. This may be momentarily relieved by the taking of food, only to become more severe by the stimulation and the hyperacid secretion that are set up by it. Liquid food may pass through the stomach without causing much annoyance, whereas solid food is always distressing. Very cold or very hot food invariably causes this gastralgia. The pain usually occurs within a half hour after ingestion. Should it not occur until an hour and a half to two hours after meals, this would justify the suspicion of an ulcer below the pylorus in the duodenum, whereas if the pain occurs at once, during the act of deglutition, an ulcer in the lower part of the esophagus should be suspected. Lying on the left side increases the pain (Leube), whereas absolute quiet and resting on the back relieve it. Pyrosis . — There is in most cases a very annoying burning feeling in the left hypochondrium and epigastrium, frequently rising to the throat. Some patients locate it posterior to the sternum, or even between the shoulder-blades ; this so-called “ heart-burn ” is caused by irritation of the stomach and esophagus by excessively acid gastric contents. If the burning is very marked in the esophagus, we may presume that abnormal peristalsis of the stomach and in- sufficiency of the cardia are cooperative in bringing about the pyrosis. The Condition of the Appetite . — In our experience the appetite is either normal or increased in the majority of cases. The instances where the appetite is positively lost are very rare. Before accept- ing a state of anorexia it is necessary to distinguish whether food is refused because the patients have no feeling of hunger, or whether they will not eat because they dread the pain caused thereby. Thirst is usually increased, and the tongue is clean. Vomiting . — The irritation and the hyperacidity set up by the presence of the ulcer cause increased peristalsis and antiperistalsis. The peristaltic unrest is accompanied by a feeling of boring undu- lation in the epigastrium. It may involve the intestine, causing gurgling, rumbling noises. The rapid evacuation of the stomach, caused by the intensified peristalsis, is rather favorable to recovery, because it brings on a speedy return of the contracted state which 33 Soo ULCER OF THE STOMACH. favors approximation of the edges of the ulcer and healing. When the pylorus is tightly closed by spasmodic contraction, the food masses remain much longer in the stomach, and the mucosa is excessively irritated by the intensely acid contents. The stomach is then distended by the constant afflux of gastric juice and saliva; also by the aspiration of air, which occurs frequently in these con- ditions. The distention causes a drawing apart of the edges of the ulcer, pain, antiperistaltic movements, and eventually vomiting. Pylorospasm is a very grave accompaniment, since it gives rise to gastric hemorrhages and new erosions by the development of the conditions just described. The vomited matter generally shows a good digestion of proteids and imperfect digestion of carbohy- drates. Hematemesis . — This is probably the most characteristic sign of ulcer. It only occurs in about half the cases. Jaworski and Korczynski (loc. cit.) assert that the acidity is very much increased immediately before and after the hematemesis. This, of course, would explain the digestion of the blood and the conversion of oxyhemoglobin into hematin hydrochlorate. The amount of the vomited blood does not give a correct impression of the degree of the hemorrhage, because considerable quantities of the blood escaping into the stomach reach the intestine and are passed out in form of tarry stools. The intestinal evacuations may contain blood several days after the hematemesis. The production of gastric hemorrhage is favored by bodily movement, but it may occur during rest, even during sleep. When very small quantities of blood escape into the stomach, they mix with the contents, are partially digested, and eventually come up in the form of coffee-ground material. When larger vessels are corroded by the ulcer, we have copious hemorrhages of dark- red, pure blood. A profuse hemorrhage, therefore, as a rule, points to a deep ulcer. Gastric hemorrhages are accompanied by the systemic phenomena of internal hemorrhages in any other part of the body, such as sinking of arterial pressure, marked pallor, sensations of warmth and pain in the stomach, cardiac oppression, nausea, cold sweat, fainting, and collapse. Death has been known to occur in the state of collapse before any blood was vomited, the stomach containing at the autopsy enormous quantities of liquid and coagulated blood. In one case a solid blood-clot filled the entire stomach. Bodily exertions, the external application of force of any kind to the region of the stomach, and straining at stool RELATION OF HYPERACIDITY AND PEPTIC ULCER. 50 have repeatedly been reported as the direct causes of gastric hemorrhage. In patients with persistent pain in the stomach, and dark-colored stools, the latter should be examined for blood- coloring matters by testing for the hemin crystals. Iron, bismuth, tannic acid, tea, claret, and huckleberries may produce a black color of the stools, and must be excluded in the diagnosis. The Relation of Hyperacidity and Peptic Ulcer. — Hyperacidity (as an etiological factor). — In the second volume of Reynolds’ “System of Medicine,” page 930, W. Fox expresses the opinion that the cause of chronicity of ulcer may be “ an excessive acidity or secretion of the gastric juice, particularly when the stomach was empty.” But to Riegel belongs the credit of having placed this condition of hyperacidity with gastric ulcer upon a scientific basis. His results were confirmed by von den Velden, Jaworski, Kor- cynski, Ewald, and Boas. According to my experience, hyperacidity is present in 90 per cent, of undoubted gastric ulcers. Riegel at first asserted that it was a constant accompaniment (F. Riegel, “ Beitrage zur Diag- nostik d. Magenkrankheiten,” “ Zeitschr. f. klin. Med.,” Bd. xii, S. 434). But Gerhardt, Rosenheim, Ritter, von Mehring, Cahn, and Hirsch published cases of gastric ulcer with normal and even subnormal acidities. We have thoroughly tested the method of analysis of Cahn and v. Mehring, and assured ourselves that it gives values that are too low for the free HC 1 , which may explain, in part, some of the results and discrepancies of Rosenheim and the originators of the method. We do not deny that there are undoubted cases of gastric ulcer in which there is a subnormal amount of HC 1 , but they are exceed- ingly rare. (This may come about as a result of exhaustion of the gland-cells consequent upon continued supersecretion. See p. 334.) Whenever the glandular layer is intact, it is reasonable to expect hyperacidity, because the presence of an ulcer is a never-ceasing irritation. Riegel has argued that the hyperacidity is a primary causative disturbance and the ulcer a secondary result of this, but Ewald’s opinion is that the reverse may be possible, and that in individuals with great irritability of the secretory nerves an injury to the mucosa may secondarily bring about the hyperacidity. Although this view of Ewald’s is plausible, — and we do not wish to deny the possibility of the hyperacidity being a secondary result in excep- tional cases, — nevertheless the results of experiments on animals 502 ULCER OF THE STOMACH. are opposed to such a conception. Many injuries to the mucosa, hemorrhagic erosions, etc., lead to recovery and do not cause peptic ulcer; only in individual cases do ulcerations develop. In experimental injuries that were produced in the stomachs of animals by Cohnhein and Matthes it was found that prompt heal- ing occurred; but the healing process was very much prolonged if hyperacidity was artificially caused by continued addition of HC1 to the contents of the stomach. On the other hand, hyperacidity was never caused by these injuries secondarily, although some ot them were very extensive. That a mechanical injury to the stomach can not of itself pro- duce hyperacidity, and thus be converted into a peptic ulcer, is proved by the cases where human beings swallowed such things as knives, bits of glass, nails, etc., and still no ulceration was found at the operation or autopsy. If this kind of trauma in a stomach previously healthy can not produce peptic ulcer, one must naturally assume that a special predisposition must previously exist if such an ulcer shall develop. It can hardly be accepted that this kind of a disposition should develop at the moment an injury is received. I have personally observed the continuance of the hyperacidity after the ulcer was healed, and I agree with Riegel in the opinion that the hyperacidity is the primary disturbance, and its continuance explains the frequent returns of peptic ulcers after supposed cures had been effected. In stomachs that show hyperchlorhydria the normal digestive stimulation of food is followed by an excessive production of HC1. If an individual afflicted in this manner receives an injury to the gastric mucosa leading to an erosion, this will not heal as it would in a healthy person, for the hyperchlorhydria that occurs every time food is taken into the stomach will prevent the healing ; more than that, it will in itself be a factor for further destruction in the injured area. Nauwerck and D. Gerhardt have recently demonstrated the transition of hemorrhagic erosions into ulcerations. Any necrosis in the mucosa may lead to an ulcer. A slight hemorrhagic infiltration may be the first step in the process, and later the infiltrated area becomes necrosed. Then the necrotic tissue is dissolved under the influence of the hyperchlorhydria. Two factors, then, are essential — hemorrhagic infiltration and a very active hyperacid gastric juice. Nauwerck has pointed out that erosions may also be a secondary result caused by mycotic and bacterial necroses of the'mucosa. RELATION OF HYPERACIDITY AND PEPTIC ULCER. 503 Inasmuch as the ulcer is not the cause of the hyperacidity, but rather the result, one can not be surprised to find occasionally that ulcer cases are not accompanied by hyperacidity. These are the exceptions. As a rule, it can be stated that gastric ulcer is asso- ciated with hyperacidity. The state of the bowels is mostly that of persistent constipation; sometimes the evacuations are normal ; this is generally the case when much water has been ingested to quench the intense thirst. The small quantity of the evacuations is explained by the fact that very little food is ingested, and this is so thoroughly dissolved in its proteid constituents by the very active gastric juice that little work remains for the intestine. Often the pylorospasm, the cicatricial contraction of the pylorus, and the frequent vomiting are agents in producing constipation, because they prevent the transit of the food into the duodenum. Colitis and membranous dysentery may coexist with gastric ulcer in rare instances. The urine is very much diminished in quantity, and is frequently highly acid when no emesis has occurred ; but when there has been much vomiting, or when the stomach has been washed out frequently, the urine may become alkaline. Maly and Quincke have observed that the excretion of the alkaline constituents of the blood goes hand-in-hand with the increased acid secretion of the stomach ; at the same time the total chlorids of the urine are very much reduced. The results of Charles E. Simon (loc. cit.) indicate that exact analyses of the urine respecting its alkalinity, the sub- normal amount of chlorids, and the excess of indican, etc., may eventually instruct us concerning the secretory processes in the stomach, where it is impossible to obtain the gastric contents for examination. (For detailed information see chapter on The Urine in Gastric Diseases.) The development of tumor or palpable swelling is a very rare occurrence in gastric ulcer cases. Very old ulcers may show con- siderable thickenings at the edges, which at times become palpa- ble. Gerhardt has described the following varieties of palpable gastric ulcer indurations or tumors : (i) The ulcer itself, with its hard base and indurated edges, is palpable. This can only be felt if it is located in that small area of the anterior gastric wall that can be palpated. Gerhardt stated that in some cases the induration could be felt through the left lobe of the liver. I have never observed a case of indurated peptic ulcer, either clinically or at autopsy, at which such palpation was possible. The existence of gastric tumor, 504 ULCER OF THE STOMACH. as a rule, speaks against ulcer and for carcinoma; but in painful gastric affections of over two years’ standing the existence of a small narrow tumor speaks for ulcer. (2) In cases of hyperacidity and gastralgia a functional hypertrophy of the pyloric musculature may develop and become palpable ; this occurs most frequently when the ulcer is located at the pylorus. This type is only palpa- ble if the stomach is dilated or prolapsed. If the pylorus is in its normal position, it can not, in my experience, be palpated. (3) After a gastric ulcer has perforated, a tumor mass may develop on the outside of the stomach by an exudate, or an encapsulated abscess may form. In these extremely rare cases a rapidly devel- oping tumor mass develops after a long-standing gastric disease, and is very likely to be mistaken for a carcinoma. (4) Old large peptic ulcers frequently envelop neighboring organs with their broadened bases. It is claimed that pancreas, spleen, and left lobe of the liver may project into the ulcer, the projecting part becoming chronically inflamed, hard to palpation, quite massive, and even capable of growth. The demonstration of excess of HC 1 in the stomach contents will prevent the diagnosis of cancer in these cases. In sixteen cases of tumor in connection with gastric ulcer, re- ported by Reinhard, six were, at autopsy, found to be due to cica- tricial stenosis of the pylorus, six to adhesions of the stomach with adjacent organs,^one to an encapsulated abscess, and three to for- eign bodies (hair, vegetable debris, lime, etc.). Diagnostic Pain Points . — Of these, there are two that are of im- portance : ( a ) the epigastric ; ( b ) the dorsal. The epigastric pain point is in the median line, or slightly to the left, very rarely to the right of it. It can not be correctly called a point, because the pain is more or less diffuse, at times spreading over an area as large as the palm of the hand. The exact limitation of the epigastric painful area varies with the location of the stomach. In most cases it is close to the xyphoid cartilage, but it may be several centimeters below that in cases of descent of the stomach, gastroptosis, dilatation, etc. The pain area described by Head (“ Brain,” 1896) as a reflected pain in gastric disease is localized by him as a small triangular spot in the left epigastrium. The pain in Head’s epigastric triangle is elicited on the slightest touch, and is not discovered if pressure is used, such as is necessary to localize the pain spots of ulcer. The epigastric pain, which is very sharply circumscribed and CLINICAL FORMS OF GASTRIC ULCER. 505 intense, may be associated with a sensation of throbbing and pulsation. The dorsal pain region, which was first described by Cruveilhier, is also sharply circumscribed. It was found in about one-third of our cases at a level with the tenth to the twelfth thoracic vertebra. Its lateral extent amounts to from two to three cm. and its vertical extent from two to five cm. In very rare in- stances there is a painful zone corresponding to the fourth or fifth thoracic vertebra. Usually, the dorsal pain point is only present on the left side, and Boas mentions a case in which the dorsal pain was present and no epigastric pain complained of. The only gastric sensation this patient had was a feeling of pressure after the ingestion of food. There was no vomiting and no blood in the stools. Pressure on the epigastric region did not cause pain, but there was an intensely painful spot at the level of the twelfth dorsal vertebra. The patient later on suffered from severe hematemesis. The localization of pain is, in our experience, only exceptionally of diagnostic aid. The so-called pain points are frequently absent, or, if present, they are not in the places designated by Boas. Neurasthenic patients often have pain points in these locations without any other evidence of ulcer. Clinical Forms of Gastric Ulcer. — 1. Hemorrhagic Form . — This type may be acute or chronic. In the acute type there are, as a rule, no well-marked symptoms of gastric ulcer, which runs a latent course, until suddenly a severe gastric hemorrhage makes the diagnosis clear. The patient may die as a result of a profuse loss of blood. If the hemorrhage does not result in death, an intense anemia remains. In the chronic type the loss of blood is not so considerable, but the hemorrhages occur more frequently. I have personally observed a case in which twelve hemorrhages occurred in one year, and the stool contained blood at all times during that year. Such cases become extremely cachectic, and pernicious anemia has been known to result. 2. The Gastralgic Form . — This type is frequently confounded with purely nervous gastralgia and the attacks of pain occurring in cholelithiasis. 3. Acute Perforating Type. — The ulcerative process runs a latent course, showing only slight dyspeptic symptoms. The acute per- foration in most cases occurs suddenly and generally ends fatally. 4. Chronic Dyspeptic Form. — This type gives the impression of chronic gastritis or nervous dyspepsia ; symptoms of gastric ulcer are wanting. The epigastric region may be sensitive to pressure, 5°6 ULCER OF THE STOMACH. and there may be vomiting and pain occurring occasionally after eating, but they are not the characteristic sharp pains peculiar to typical ulcer; they partake more of the discomfort shown in other chronic diseases of the stomach. If such cases show ex- cess of HC1 in the gastric contents, and no abundance of mucus, the diagnosis will most probably be ulcer. 5 . The Cachectic Form . — These very emaciated and cachectic patients frequently give the impression of being afflicted with a cancer. The condition is most frequently seen in advanced stages of long-existing ulcers, in dilatations caused by cicatrices, or in chronic cases of hypersecretion. Attacks of pain and vomiting are still present, but the general appearance is that of cachexia and even marasmus. 6 . Vomitive Form . — Here the emesis is the most annoying symp- tom, which is so persistent that the sufferers rapidly assume an advanced stage of emaciation. These types of gastric ulcers are sufficient to demonstrate how variable the clinical picture may be. The Duration. — It is impossible to determine how long a gastric ulcer has existed, and it is difficult to determine when a complete cure has been effected. Even the cessation of pain is no proof of perfect healing. Large gastric ulcers, with extensive lateral and vertical destruction, probably never heal perfectly. As a rule, the disease runs a chronic course. There are cases that DESCRIPTION OF PLATE VIII.— ULCUS CARCINOMATOSUM OF THE PYLORUS. Fig. 1. — A Section Through the Wall of the Stomach, Showing the Edge and a Portion of the Base of the Ulcer. Objective, two-thirds ; eyepiece, two inches. Stained with hematoxylin and eosin. The drawing is built up from a series of microscopic fields. X a bout 15 dia- meters. d. Mucous membrane, m. Muscularis mucosae, s. Submucosa, a. Base of the ulcer, mm. Muscle-coat of stomach, me. Groups of cancer cells between the bundles of muscle-fibers, dc. Groups of cancer cells in the edge of the ulcer in the mucous membrane. sc. Groups of cancer cells in the submucosae. a. Necrotic membrane lining the base of the ulcer. Fig. 2. — A Small Nodule from the Serous Coat of the Stomach Over the Base of the Ulcer. Objective, two-thirds ; eyepiece, two inches. Stained with hematoxylin and eosin. X about 15 diameters. This figure gives a good idea of one of the nodules in the serosa. It is composed entirely of a collection of groups and masses of cancer cells, so closely packed that the outlines of the individual cells can not be made out. Except for these nodular thickenings, the serosa was not altered, pc. Cancer masses in peritoneal coat. PLATK VIII. DIAGNOSIS. 507 run an acute course and become perfectly healed within a period of from four to six weeks. The long duration of the majority of cases is largely explained by the irritating character of the food and by the late recognition of the character of the trouble. Com- plications may greatly prolong the disease. The course is a very variable one, and a complete cure should not be spoken of until the patient has been perfectly free from all gastric distress for six months. In some cases the symptoms may disappear very rapidly under strict diet and appropriate treatment. After a few weeks, months, or years the same symptoms return. The question now arises whether this has been caused by a new ulcer or whether the old ulcer has not yet healed. It is almost impossible to decide this point, though it is probable that the old ulcer has not yet been perfectly cured. This is particularly the case if the distress has only been relieved as long as the patient strictly keeps to a careful diet. If the pains recur whenever an ordinary diet is taken, the case is not cured. The hyperacidity may continue after the ulcer has been cured, but need not neces- sarily cause a relapse. Diagnosis. — If the symptoms of pain in the stomach, gastric hemorrhages, and hyperchlorhydria are present simultaneously, the diagnosis is assured ; but in the majority of cases pain is the only symptom. If the pain occurs only at the height of digestion and at a circumscribed area in the epigastrium, and if the dorsal pain point is present, gastric ulcer should be suspected. Hyperchlor- hydria, in connection with continued pain, should also suggest ulcer. The pain or cardialgia of hyperchlorhydria is sometimes indistinguishable from that of gastric ulcer. Both kinds of pain are caused by the digestive irritation of the food. Both cease when the ingesta have left the stomach. The only important point of difference between these two pains is their regularity with ulcer and their irregularity in hyperchlorhydria. In the latter there may be days in which the patients are entirely free from pain. In doubtful cases it is always safe, according to Leube’s plan, to insti- tute treatment for ulcer. 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 cer- tain ( loc . cit.y p. 41). He attributes less importance to analysis of the gastric contents. There are, however, atypical forms which present some difficulty in diagnosis. Thus there are cases rarely 508 ULCER OF THE STOMACH. observed in which the patients never complain of pain, nor has the food any distressing effect upon the stomach. In other cases, although pain is present, it is not aggravated by taking food. In some well-diagnosticated cases food of all kinds was well borne. In all of these well-authenticated forms the diagnosis was assured by characteristic unmistakable symptoms, such as hematemesis and bloody stools, coming on afterward. Concerning hematemesis, it should be said that the differentiation of pulmonary from gastric hemorrhage may become necessary. This may be facilitated by a study of the subjoined scheme: HEMORRHAGES FROM THE Lung. Stomach. 1. Blood is bright red, foamy. 2. Physical signs point to a pulmonary or cardiac affection — the stomach may be affected secondarily. 3. Pulmonary hemorrhages followed by rusty-colored sputa for days (gener- ally), but there is no blood in the stools. 4. Physical signs of pulmonary or cardiac disease — moist rales. 1. Blood is dark brown, partly coagulated, frequently mixed with food, sometimes acid. 2. Physical examination evinces a gastric or hepatic affection, or stasis in portal circulation. 3. Gastric hemorrhages are frequently as- sociated with tar-colored stools. 4. Physical examination of heart and lungs usually negative. The diagnosis becomes complete if the characteristic pain points are present, with prompt aggravation of pain soon after taking food, vomiting showing hyperacidity, hematemesis, and a history of chronic trouble. The blood coming from the stomach does not necessarily origi- nate 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, and yellow fever. 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), but Debove suggests (Joe. cit.) that organic and functional nervous diseases may be coincident with ulcer. In sudden gastric hemor- rhages 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 entirely absent. CHOLELITHIASIS. 509 Affections of the transverse colon, — some forms of colitis (mem- branous and simple catarrhal types), — as well as severe colic, coprostasis, and prolapse of the colon, may closely mimic the clinical picture of gastric ulcer. The pain area of the transverse colon can not, in my experience, be definitely separated from that of the stomach by palpation. In this connection I would empha- size that pains of the colon cease and frequently disappear entirely after this part of the intestines is thoroughly evacuated. In the greater proportion of these diseases of the colon the amount of free HC1 in the stomach is markedly reduced, or occasionally may be absent entirely. In ulcer there is hyperacidity, as a rule. Careful inspection and examination of the stool is necessary in both diseases, and will often instruct us regarding the condition of the colon. Whether colitis may lead up to functional disturbances of the stomach, as Fleiner asserts, is still uncertain. 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 hepatic colic is not in connection with the taking in of food ; it draws from the median line to the right. The dorsal pain point of ulcer, if present, is located at the level of the twelfth tho- racic vertebra, to the left and very close to the body of the twelfth vertebra. But the dorsal pain point of cholelithiasis, if present, is located to the right, about two or three fingers’ breadths from the twelfth dorsal or first lumbar vertebra. In ulcer there is rarely any pain on the right side; even if there is, it is much less intense, and in cholelithiasis there is rarely any pain to the left of the spinal column. In cholelithiasis the right lobe of the liver and the gall-bladder are enlarged after an attack; and during the intervals between the attacks all kinds of foods can be eaten with impunity. In chole- lithiasis the amount of HC1 in the gastric contents is normal or sub- normal, or the contents may not show any free HC1; in ulcer there is 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 occasionally observed. In private practice I have observed two cases in which chole- lithiasis and gastric ulcer occurred contemporaneously. Diagnosis of the Complications and Consequences of Gastric Ulcer . — These are: ( 1 ) The perforation peritonitis; ( 2 ) cicatricial stenosis 5io ULCER OF THE STOMACH. of the pylorus; (3) the transition of ulcer into carcinoma, or ulcus carcinomatosum ; (4) hour-glass stomach from cicatricial contrac- tions ; (5) subphrenic abscess ; (6) progressive pernicious anemia. The diagnostic signs of perforative peritonitis are : (a) great rigidity of the abdominal muscles, flat abdomen ; ( b ) disappearance or diminution of liver dullness; this sign may be absent, however, if only liquid gastric contents and no air escape into the peri- toneum ; ( c ) vomiting.* According to Rosenheim (“ Zeitschr. f. klin. Med.,” Bd. xvu, S. 116), about five to six per cent, of gastric ulcers develop carcinomata at their margins, and these carcinomata are said to be associated with a pronounced hyperacidity. The so-called hour-glass stomach may be produced by one or more cicatrices in the neighborhood of the antrum pylori. Cicatrices of the duodenum may cause a dilatation beyond the pylorus, by which the latter will itself constitute the narrowing or isthmus of what very much resembles an hour- glass stomach (Reiche, “Jahrb. d. Hamburger Staatskrankenan- stalt,” 1890, p. 180). Subphrenic Abscess (Pyopneumothorax subphrenicus). — In 1880, Leyden first described a combination ol 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 poste- rior and lower thoracic regions give dullness on percussion, absence of vesicular murmur, and fremitus. Metallic sounds can be made out when one percusses and auscults simultaneously. The succus- sion sound is distinct. The lung is distinctly intact above these parts. The respiratory murmur is vesicular and the fremitus is maintained down to the fourth or fifth rib ; from here on, the respira- tory 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 coordi- *The diagnosis of perforation has been attempted, when other signs failed, by punc- turing through the abdominal walls with a sterilized hypodermic needle, when the gaseous, bacterial, and cellular evidences of perforation can at times be aspirated. (Test for H 2 S by lead-acetate paper ; when the abdomen is very tympanitic, this sign is almost pathognomonic.) The puncture is made when the patient is in the dorsal position. The escaped gases will rise upward between the intestines and the peritoneal wall. There is danger of puncturing the intestines in this method. TREATMENT OF GASTRIC ULCER. 5 nated, the intercostal spaces are almost obliterated, and the heart is 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 and abundant expectoration of foamy pus containing hepatic cells. In 1894 Maydl collected 179 cases of subphrenic accumulations of pus. In twenty per cent, of these cases perforating ulcers of the stomach or duodenum were found to be the causes. (“ Subphrenic Abscess,” Meltzer, in the “ New York Med. Jour.,” June 24, 1893.) Progres- sive pernicious anemia as a concomitant phenomenon of ulcer can be recognized by the reduction of the number of red corpuscles with relative increase of percentage of hemoglobin and the appearance of the poikilocytes, gigantoblasts, microcytes, and macrocytes. (See chapter on The Blood in Gastric Diseases, p. 400 et seq.) Senator suggests that a left-sided pleurisy immediately or remotely following gastric ulcer should suggest the possibility of a subphrenic abscess. The following are further suggestive points in these cases : First, violent pains in the epigastrium, or in one or other hypochondrium. Second, pain and stiffness in the back dur- ing efforts to sit up. Third, painful eructation, sobbing and singultus. Fourth, reclining posture of the patient on his back, because, as a rule, with extensive pleuritic extravasations the patient maintains a position on the diseased side. Fifth, edema of the lower lateral and posterior thoracic walls, at times extending to the loins. In the presence of extensive pleurisy or empyema, the coexist- ence of these five conditions would justify the supposition of a subphrenic abscess. The general subcutaneous emphysema as a complication of perfor- ation of gastric ulcer is a very rare occurrence, to which Demarquay first called attention. Treatment of Gastric Ulcer. — Prophylactic. — If gastralgias are frequent in a person afflicted with hyperacidity, the diet must be very mild and unirritating; two weeks of a milk diet will be the safest. Sudden deviations in the temperature of the food must be avoided, daily evacuations must be effected by suitable diet, and, if need be, Carlsbad salts, and the hyperacidity remedied. The dietetic and medicinal treatment will vary according to the presence or absence of hematemesis. Treatment of Hematemesis and the Period Immediately Follozving It. — During the stages of blood vomiting the patient must remain 512 ULCER OF THE STOMACH. absolutely quiet in bed and not even arise for urination or defeca- tion. 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 anemic, a nourishing enema may be imperatively indicated every four hours. The enema most favored is that of Boas, consisting of 250 gm. of milk, the yolks of two eggs, a teaspoonful of salt, one ounce of good claret (we favor Beaune-Burgundy for this purpose), and one tablespoonful of aleuronat flour. Previous to giving an enema for nutritive pur- poses, the rectum and colon must be cleaned by a high irrigation with one liter of warm water. The above ingredients are thor- oughly mixed by means of an egg-beater, warmed to about 99 0 F., and permitted to run in under gentle pressure, care being taken that the tube is introduced as far up into the sigmoid flexure as possible. When the hematemesis is copious and persistent, a hypodermic injection of ergotal, 20 to 30 minims, should be given at once. With this preparation of ergot we have had extensive experimental and clinical experience (see “Med. News” for Jan. 31, Feb. 7, Mar. 7 and 14, 1891, “An Experimental and Clinical Study of Ergot,” by J. C. Hemmeter). The use of ergot for hematemesis has the indorsement of Riegel (loc. cit.), Ewald, and Nothnagel. At the same time an ice-bag is placed over the epigastrium, and if the pain is severe an injection of of a grain of morphin should not be delayed, as this drug acts as an adjuvant to the hemostatic by the ease and quiet it brings about. For three days following hematemesis this treatment should not be changed, and no food allowed by mouth. The treatment from the fourth to the seventh day after consists of absolute rest in bed, a wet pack covered with oiled silk and bandage being applied to the epigastrium. 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 nutrose, meat-powder, or somatose have been added, and egg- albumen water. Chocolate, yolks of eggs, and all alcoholic beverages must be forbidden in this stage. In the second week after the hemorrhage a typical cure for ulcer, according to principles laid down by Wilson Fox (“ Diseases of the Stomach,” 1872, p. 146), v. Leube (“ Ziemssen’s Handbuch,” Bd. TREATMENT OF GASTRIC ULCER. 513 vii, 2, p. 120), and v. Ziemssen (Volkmann’s “ Sammlung klin. Vor- trage,” No. 7 5), should be instituted. These systematic treatments are in the main rest-cures combined 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 Miihlbrunnen in which five to ten gm. of natural or artificial Carlsbad salts have been dissolved. Spongiopi- lin cut into any requisite shape and dipped into hot water is applied externally to the epigastrium, and renewed every three hours night and day. The diet consists mainly of milk and whipped eggs ; if there is great weakness, the Boas enema, containing perhaps two ounces of claret, should be given, and if the pulse is feeble, hypodermic injections of digitalin To of a grain, and strychnia ^ of a grain. In one case of profuse hematemesis we 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 effect 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. We might remark here that the Saratoga Carlsbad and the Hathorn spring waters act quite as well as the imported. In fact, the only objects of the Carlsbad water in the cures of Leube and Ziemssen are the neutralization of the hyperacidity and the promotion of intestinal evacuation. One must not gain the impression that Carlsbad waters or salts have any direct or specific curative effect. Ewald {loc. cit ., 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 autodigestion I usually give the fol- lowing : R . Magnesias ustae, Sodii carbonatis, Potassii carbonatis, .... aa ... . 5.0 3 j -f- grs. xv Sacchar. lactis, 25.0 3 v j T g rs - xx * SlG. — Half a teaspoonful dry on the tongue every three hours. In the third week one may permit dipped cakes, toast, or zwie- back ; broiled sweetbread or calf’s brain, dumplings made of finely divided meat, broiled pike, bluefish, trout, oysters, in very small quantities. In the fourth week purees made of potatoes, peas, or 34 5 14 ULCER OF THE STOMACH. beans rubbed through a sieve, stewed apples, pears, and plums. Saratoga Vichy may be allowed; all vegetables that can be prepared in puree (gruel) form, such as spinach, carrots, peas, 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 hematemesis the treatment had best be carried out along these lines also. On page 241 detailed diet-lists for cases of gastric ulcer are given. In rebellious cases of recurrent gastralgias, vomiting, and hyperacidity, McCall Anderson (“Brit. Med. Jour.,” May 10, 1890) and H. B. Donkin (“The Lancet,” Sept. 27, 1890) recommend a total abstinence cure of two to three weeks, during which the patients are fed exclusively by rectal enemata (three to four in the day); hot applications to the epigastrium are also used. After ten days of rectal feeding they cautiously and slowly return to feeding by the mouth (milk, bouillon, egg-albumen). We have tried this in a number of cases in which relapses had occurred after the rest-cure, and can speak in favor of the method. (See, also, A. P. Gros, “ Traitement de Malad. de l’estomac, par la cure de Repos absolu,” etc., Paris, 1898.) Gerhardt and Boas speak very favorably of nitrate of silver in light cases of gastric ulcer. The latter begins with: 3 ^. Argenti nitratis 0.25 to 120 of peppermint water; one tablespoonful three times a day on an empty stomach. Then the dose is increased to 0.3 to 120 of water, of which two bottles are taken, and finally 0.4 to 120 of water, of which also two bottles are advised. This is combined with a sparing diet and as much rest as possible. Fleiner and Kussmaul recommend bismuth subnitrate in all irritative conditions of the gastric mucosa — old ulcers, erosions, excoriating carcinomata. Fleiner employs it in the following manner: 10 to 20 gm. (150 to 300 grs.) of bismuth subnitrate are 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 three 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 local treatment. We usually employ three drams of bismuth subnitrate and one dram of bismuth subgallate in a pint of warm water, having previously thoroughly cleansed the stomach with solutions of sodium bicarbonate (5ss to a pint), the state of the ulcer permitting. Recently we have used the bismuth salts by insufflating them into the stomach in a dry form by a powder blower. SURGICAL TREATMENT OF GASTRIC ULCER. 515 In chronic cases in which Fleiner’s treatment can be employed it relieves pain promptly, reduces the hyperacidity, and promotes healing; it is worth trying in cases of long standing. Direct or local treatment of this kind is permissible when there have been no hemorrhages or tarry stools for one month. During this time the ordinary cures by diet, rest, Carlsbad Miihlbrunnen, etc., must have been employed. There must be no sensitiveness to pressure on the epigastrium. Chronic ulcers that have resisted dietetic and medicinal treatment have been successfully treated by this method by Matthes (loc. cit.), O. Fischer ( loc . cit.), and Stintzing (Joe. cit .). The anemia following ulcer may require iron, arsenic, strychnin. Iron preparations must contain no acid. J. Petruscky has reported two cases of primary tubercular ulcers of the stomach which were apparently cured by injections of tubercu- lin (“ Verhandlung d. XVII Congress f. innere Med.,” 1899, S. 366). Surgical treatment becomes necessary when, after a trial of the aforesaid methods, the ulcer or ulcers prove very obstinate and not amenable to medical treatment, or because hemorrhages may be- come so abundant and frequent as to endanger life, or, lastly, because of perforation. Nelson C. Dobson (“ Bristol Medical and Surg. Jour.,” 1883) first advocated surgical interference for per- forating gastric ulcer. In this country, Robert F. Weir, of New York, has contributed the most important work to this domain of surgery. His last important paper (Robert 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, 1896) contains an account of 78 cases of laparotomy for acute perforation of gastric ulcer. Keen and Tinker have added statistics of 78 further cases (“ Phila. Med. Jour.,” vol. 1, p. 1106); these articles contain also the indications, prognosis, etc., of operations for gastric ulcer. Gastric ulcers have been excised entirely, the sequelae thereof have been removed by the severing of peritonitic adhesions, and hour-glass stomach much improved by gastro-anastomosis (see von Hacker, “ Ueber Magenoperationen bei Carcinom u. b. narbigen Stenosen,” published by Wilh. Braumuller, Wien and Leipzig, 1895). For further details concerning the operations on the stomach for recent ulcers and for cicatrices, we refer to the sections on Sur- gery of the Stomach. Treatment of Exhaustive Gastric Hemorrhage by Transfusion and Intravenous Injection of Normal Salt Solution. — Michel transfused 5 16 ULCER OF THE STOMACH. successfully in a case of extreme anemia following gastrorrhagia (“ Berl. klin. Wochenschr.,” 1870, No. 49). In a case of profuse and repeated hematemesis, which followed washing out the stomach, Michaelis infused into the veins 350 c.c. of solution of common salt. Reaction gradually followed, and the patient recovered. This case, which was one of probable ulcer, illustrates the advantages of infus- ing a small quantity {ibid., June 23, 1884). The sudden infusion of quantities of liquid exceeding 500 c.c. will cause such an abrupt rise in arterial pressure that the injured blood-vessels in the gastric mucosa may reopen, causing renewed profuse hemorrhages. The dangers are illustrated by a case reported by von Hacker, who infused 1500 c.c. of salt solution into a patient in a state of extreme collapse resulting from hemorrhage from gastric ulcer. The patient rallied, but he died three hours after the infusion from renewed hemorrhage (“Wiener med. Wochenschr.,” 1883, No. 37). In Legroux’s case of gastric ulcer, renewed hemorrhage and death followed the transfusion of only 80 gm. of blood (“Arch. Gen. de Med.,” Nov., 1880). In a case quoted by Roussel, Leroy transfused 130 gm. of blood into a girl twenty years old, who lay at the point of death from repeated hemorrhages from a gastric ulcer. In the following night renewed hemorrhage and death occurred (“ Gaz. des Hop.,” September 22, 1883). According to the experiments of Schwartz and Ott, the transfusion, or, rather, infusion, of physiological salt solution is as useful as that of blood, and it is simpler and unattended with some of the dangers of blood transfusion. The formula is chlorid of sodium, 6 parts; distilled water, 1000. Our personal experience is confirmatory of the observations of these last-mentioned ex- perimenters. Fleiner ( loc . cit .) favors the excision of simple gastric ulcer, when external (social) conditions render a suitable diet and treatment impossible. We can not advocate this heroic treatment for simple, uncomplicated ulcer, feeling convinced that the various treatments with which we are now acquainted are eminently successful. But if a laparotomy has been undertaken and the stomach has been opened for other indications (suspicion of peritonitis, perigastritis, appendicitis, carcinoma, perforation), and an uncomplicated ulcer is discovered, the excision of the latter is undoubtedly justifiable, and has been successfully carried out by Cordua, Kansche, Maurer (at Czerny’s clinic), and Mintz {loc. cit.). In the latter case the gastric functions were entirely recovered. Extreme and persistent gastric LITERATURE ON ULCER OF THE STOMACH. 517 pain has been the indication for gastroenterostomy in a case of Cahn’s ( loc . cit.). LITERATURE ON ULCER OF THE STOMACH, In addition to the text-books mentioned in the literature on gastritis. 1. Abaytia, W., “ Trataimento de la ulcera heptica en plena actividad gastrica mitigado por la alimentacion rectal,” “ Rev. de med. y cirug. pract.,” Madrid, 1898, xliii, 401, 489, 529. 2. Adamson, R. O., “ The Symptoms of Perforated Gastric Ulcer, with Two Recent Cases,” “ Scot. M. and S. J.,” Edinb., 1898, 11, 317-326. 3. Affleck, J. O., “ Edinburgh Hospital Reports,” 1894, vol. 11, pp. 198-238. 4. Alexander, W. C., “A Case Illustrating the Difficulty of Diagnosis in Gastric Ulcer,” “Brit. M. J.,” 1897, 1, 1345. 5. Allen, J. E., “ Hereditary Influence or Family Tendency as a Predis- posing Cause of Gastric Ulcer,” “Yale M. J.,” New Haven, 1897-98, iv, 229- 232. 6. Altmann, J. F., “ Ulcer of the Stomach,” “ Tr. M. Soc. Tennessee,” Nash- ville, 1898, 105-113. 7. Anderson, “ British Medical Journal,” May 10, 1890. 8. Anderson, G. R., “Note on a Case of Perforated Gastric Ulcer,” “ Brit. M. J.,” Lond., 1898, 1, 1448. 9. Ardouin, “Ulcere d’estomac, Gastrotomie,” “Soc. Anat.,” 17 Dec., 1897. 10. Assaky, “Ulcer stomacal,” “ Spitalul Bucuresci,” 1898, xvm, 77-84. 11. Auffray, “Contribution a l’etude, du diagnostic de la peritonite suraigne dans l’ulcere perforede l’estomac,’’ “ These de Paris,” 23 Juin, 1896. 12. Barling, “ Birmingham Medical Review,” August, 1895. 13. Beck, C., “ Medical Record,” Feb. 15, 1896. 14. Begouin, “Ulcere latent de l’estomac ; perforation; mort,” “ Journ. de med. de Bordeaux,” 24 Jan v., 1897. 1 5. Bellrose, N. W., “ Gastric Ulcer, Probably Tubercular, Report of a Case,” “ Colorado M. J.,” Denver, 1897, III, 169-174. 16. Benedict, A. L., “ Gastric Ulcer,” “ Med. News,” N. Y., 1898, lxxiii, 675-678. 17. Bensley, C. N., “A Case of Chronic Ulcer of the Stomach,” “Indian Lancet,” Calcutta, 1897, x, 171. 18. Berg, A. A., “The Etiology of Gastric Ulcer and an Outline of Its Therapeutics,” “ Med. Record,” July 30, 1898. 19. Bernardbeig, “ De l’Ulcere de l’Estomac,” “Normandie Med.,” Rouen, 1897, XII. 20. Blackader, A. D., “Gastric Catarrh and Gastric Ulcer,” “ Am. Text- book Dis. Child.” (Stan.), 2d ed., Phila., 1898. 21. Bohland, “ Ueber die Hernia epigastrica und ihre Folgezustande,” “ Berl. klin. Wochenschr.,” 1894, No. 34. 22. Bondet, “ Gastrorrhagie par Ulcere de l’Estomac, Traitement,” “ Province Med.,” Lyon, 1898, xn, 380-383. 23. Borchgrevink, “ Ulcus Ventriculi Perforatum, Laporotomie,” “ Norsk. Magaz. f. Laegevidensk,” 1897, Heft. 1. ULCER OF THE STOMACH. 24. Bottcher, A., “ Zur Genese des perforirenden Magengeschwiirs,” “ Dorpat. med. Zeitschr.,” 1874. 25. Bramwell, B., “Clinical Remarks on a Case of Acute Perforative Peritonitis Due to Ulceration of the Stomach,” “ Internat. Clin.,” Phila., 1898, 8 s., 1, 1 16-122. 26. Brenner, “Zur Magensecretion bei Ulcus ventriculi,” “Wiener klin. Wochenschr.,” No. 48, 1897. 27. Brinton, W. {Joe. cit.). 28. Broadbent, W., “ Perforated Gastric Ulcer,” “Brit. M. J.,” Lond., 1897, hi, 1254-1257. 29. Bugge, “ Ulcer of the Stomach Causing Death by Internal Hemorrhage,” “ Forh. med. Selsk. i. Kristiania,” 1897, 203-205. 30. Bush, J. Paul, “Cases of Perforative Gastric Ulcer Treated by Opera- tion,” “Brit. M. Jour.,” Nov. 5, 1898. 31. Cabot, A. T., “ A Case of Perforating Gastric Ulcer ; Operation at End of Twenty-four Hours; Recovery,” “Boston M. and. S. Jour.,” Aug. 11, 1898. 32. Cade, “Ulcere Perforant de l’Estomac Chez un Enfant de Deux Mois,” “ Soc. des Scienc. med. de Lyon,” Oct. 20, 1897. 33. Cahn, “ Berlin, klin. Wochenschr.,” 1894, No. 28. 34. Campbell, J., “A Case of Operation for Perforated Gastric Ulcer,” “ Brit. med. Journal,” July 16, 1898. 35. Caro, “ Ueber Blutungen aus Oesophagusvaricceen,” Diss., Wurzburg, Heidelberg, 1896. 36. Cathcart, C. W., “Ruptured Gastric Ulcer,” “Tr. Med.-Chir. Soc.,” Edinb., 1896-97, n. s., xvi, 195. 37. Caussade, “Ulceration Gastrique, Hematemese Foudroyante, Mort,” “ Presse. Med.,” 30 Janvier, H. 9. 38. Chaput, “ Traitement des Ulceres Gastriques,” “ Gaz. de Hop. Par.,” 1898, lxxi, 67. 39. Chaput, “ Ulcere Gastrique avec Tumeur Volumineuse, Gastro-enteros- tomie, Disparition des Accidents et Persistance de la Tumeur,” “ Soc. Med. des Hopitaux,” 31, 1, 1897. 40. Chauffard, “Ulcere Simple de l’Estomac avec Hemorrhagies Abon- dantes, Guerison ; Mort par Coma Diabetique,” “Jour de Med. et Chir. Prat.,” 10 Mar., 1898. 41. Choppin, “ De la Perforation dans l’Ulcere Latent d’Estomac,” “ These de Paris,” 1896. 42. Claisse, “ Ulcere Rond del’Estomac; Perforation; Peritonite Suraigue, Mort,” “Soc. Anat.,” Paris, 8 Janvier, 1897. 43. Clubbe, C. P. B., “ Four Cases of Operation for Perforated Gastric Ulcer,” “Austral. Med. Gaz.,” June 20, 1898. 44. Connelly, A. W., “ Ulcer of the Pyloric Orifice,” “ Intercolon. M. J. Austral.,” Melbourne, 1898, ill, 536-538. 45. Cramer, “Ueber die Behandlung des Ulc. ventr. mit gross'en Wismuth- dosen,” “ Miinchener med. Wochenschr.,” 1896, No. 25. 46. Cruveilhier, “ Anatomia Pathologique,” 1829-1835, Livraison x. 47. Czygan, “Zur Behandlung der ulcusartigen Magenerkrankungen,” “ Therap. Monatsschr.,” Berk, 1898, xil, 494-496. 48. Debove et Remond, “ Traite des Maladies de l’Estomac,” Paris, p. 255. LITERATURE ON ULCER OF THE STOMACH. 519 49. Decker, “Exp. Beitrag zur Aetiologie der Magengeschwtire,” “Berl. klin. Wochenschr.,” 1887. 50. Diddens, E. J., “ Een paar complicatier van het maagulcus en haar- chirurgische behandeling,” “ Nederl. Tijetschr. v. Geneesk.,” Amst., 1898, 2 R. xxxiv, d. 2, 441-453. 51. Dieulafoy, “Ulcdres Latents de l’Estomac,” “ Presse Med.,’’ 25, vii, 1897. 52. 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Etienne, “ Ulcere latent,” “ Soc. de Med. de Nancy,” 11, xi, 1896. 62. Ewald, C. A. ( loc.cit .), p. 234; “ Diseases of the Stomach,” p. 233. 63. Ewald, C. A., “ Klinik der Verdauungskrankheiten,” 1. Theil, 3. Aufl., p. 122. 64. Fanoe, “ Fall von Ulcus perforans ventriculi, durch Laparotomie und Sutur geheilt,” “ Hospital stidende,” 52, 1896 (Casuistik). 65. Fenwick, C., “ A Case of Gastric Ulcer Perforating into the Pericardium,” “ Lancet,” Lond., 1897, 11, 388. 66. Fenwick, W. S., “ Ulcer of the Stomach in Children,” “ Internat. Clin.,” Phila., 189 7,7 s., 11, 165-177. 67. Fischer, O., “ Bismuth Treatment,” “ Dissertation,” Jena, 1893. 68. Fisher, H. M., “ Perforating Round Ulcer of the Stomach,” “ Tr. Path. Soc.,” Phila., 1898, xviii, 46,47. 69. Fleiner, “ Verhandl. des XII. Congresses f. innere Medicin,” 1893; also “ Volkmann’s Vortrage,” No. 103. 70. Flexner. 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Horner, “ Cardialgie durch Einklemmung praperitonealer Lipome,” “ Prager med. Wochenschr.,” 1892. 96. Jacot-Descombes, Ch., “ Contribution anatomique a l’etude de la patho- genic de l’ulcere rond de l’estomac,” “ These de Paris,” 1897. 97. James, A., “Gastric Ulcer,” “ Internat. Clin.,” Philadelphia, 1898, 8 s., 126-135. LITERATURE ON ULCER OF THE STOMACH. 521 98. Jaworski und Korczynski, “ Deutsche med. Wochenschr.,” 1886, Nos. 47 - 49 - 99. Jonas, A. F., “Operation for Ulcus Ventriculi Chronicum, Three Cases, with Remarks on Indications for Operation,” “West. Med. Rev.,” Lincoln, Neb., 1897, 11, 285-287. 100. Jones, Eleanor C., “A Case of Gastric Ulcer Terminating in Hemor- rhage and Death,” “ Med. News,” New York, 1897, lxxi, 499. 101. Key, Axel, “ Gurlt-Virchow’s Jahresb.,” 1871. 102. Klaussner, “ Ein Beitrag zur operativen Behandlung des Ulcus ven- triculi,” “ Munch, med. Wochenschr.,” 1897, No. 37. 103. 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Vortrage,” 1892, No. 61. 120. Lincoln, J. R., “ Gastric Ulcer in the Newborn, Etiology, Maternal Impressions,” “ Boston Med. and Surg. Jour.,” 1897, cxxxvu, 178. 121. Litten, “Ulcus ventriculi tuberculosum,” “Virchow’s Archiv,” Bd. LX vi 1. 522 ULCER OF THE STOMACH. 122. Liitzeler, “ Statistisches liber Magengeschwiire und operative Eingriffe bei denselben,” Dissert., Bonn, 1895-96. 123. Luys, G., “ Ulceration gastriques chez un alcoolique mort subite par hemorrhagie,” “ Bull. Soc. Anat. de Par.,” 1896, lxxi, 660-667. 124. Lyell, “A Case of Gastric Ulcer with Perforation in Two Places,” “ Brit. Med. Jour.,” London, 1898, 1, 818. 125. Lyon, G., “ Traitement de l’ulcere simple de l’estomac,” “ Gaz. d. Hop.,” Paris, 1898, 3 s., xv, 356-358. 126. Lyon, “ Discussion sur le traitement de l’ulcere de l’estomac,” “ Bull, gen. de therap.,” etc., Paris, 1898, cxxxvi. 127. Mackenzie, J., “ A Case of Gastric Ulcer with Characteristic Seat of Pain,” “ Edinb. Med. Jour.,” 1897, n. s., II, 591. 128. Mackenzie, J., “ The Site of Pain in Gastric Ulcer,” “ Edinb. Med. Jour.,” 1897, n. s., 11, 154-158. 129. Mackenzie, W. G., “ Perforation, Ulcer of Stomach with Hour-glass Contraction,” “ Tr. Path. Soc.,” London, 1896-1897, XLViii. 130. Marcet, “ Medico-Chirurgical Transactions,” vol. xil, p. 72. 1 3 1 . Marchand, “ Gastromalacie (und CEsophagomalacie),” “ Real-Encyklo- padie,” xil. 132. Marcille, “ Ulcere gastrique ; abces de la rate, abces sous phrenique,” “ Soc. Anat.,” Paris, 10 juin, 1898. 133. Marin Perujo, “Ulceration del estomago por el uso inadecuado de la quinina,” “ Siglo med.,” Madrid, 1897, xliv, 706. 134. Matthes, “ Ueber den Vorschlag Fleiner’s, Reizerscheinungen des Magens mit grossen Dosen Wismuth zu behandeln,” “ Centralblatt fiir innere Med.,” 1894. 135. Mauwerk, C., “ Gastritis ulcerosa chronica, ein Beitrag zur Kenntnis des Magengeschwiirs,” “ Miinch. med. Wochenschr.,” 1897, xliv, 955, 987. 136. Mayer, W., “ Gastromalacia ante mortem,” “ Deutsches Arch, fiir klin. Med.,” ix, 1872. 137. McCohs, A. J., "A Case of Perforating Gastric Ulcer; Operation, Recovery,” “Med. News,” 16, 1, 1897. 138. Metcalfe, W. B., “ Etiology and Diagnosis of Ulcer of the Stomach,” Matthews, O. J., “ Rectal Dis.,” Louisville, 1897, IV, 335-344. 139. Merigot de Freigny, “Traitement de l’ulcere Gastrique par le repos absolu de l’Estomac,” “ Rev. gen, de clin. et de Therap.,” Par., 1897, xi, 5 1 7— 520. 140. Mintz, “ Operative Behandlung der Magenkrankheiten,” “ Zeitschr. f. klin. Med.,” Bd. xxv, 1894. 141. Morely, “Ulcere rond de l’Estomac devolution lente, Perforation peritonite generalisee,” “Soc. Anat.,” 10 Dec., 1897. 142. Muller, L., “ Das corrosive Geschwiir im Magendarmkanal,” Erlangen, i860. 143. Murrell, W., “Gastric Ulcer and Its Treatment,” “ Med. Brief,” St. Louis, 1898, xxvi, 673-676. 144. Neuwerck, C., “Ueber den mycotischen Ursprung des peptischen Magengeschwiirs,” “ Miinchener med. Wochenschr.,” 1895. 145. Nissen, “Zur Frage der Indication der operativen Behandlung des runden Magengeschwiirs,” “ Petersburger med. Wochenschr.,” 1890. LITERATURE ON ULCER OF THE STOMACH. 523 146. Nitka, “Ueber embolische Magengeschwiire,” Dissert., Freiburg i. Br., 1895-96. 147. v. Noorden, “ Magensaftsecretion und Blutalkaleszenz,” “Arch, fur exp. Pathologie u. Pharm.” 148. v. Noorden, “ Zwei operative Eingrifife wegen Folgezustanden von Magengeschwiiren,” “ Miinch. med. Wochenschr.,” No. 35, 1896. 149. Nolte, see Ewald {loc. cit., 239). 150. O’Donovan, C., “On the Treatment of Gastric Ulcers after Hemor- rhage,” “ New York Med. Jour.,” 1897, lxvi, 51-53. 1 5 1. Oliver, F., “ Ulceration of the Pylorus and Its Consequences,” “ Inter- nat. Clin.,” Philadelphia, 1898, 8 s., 1, 146-157. 152. Openchowski, “ Zur pathologischen Anatomie der geschwiirigen Pro- cesse im Magendarmtractus,” “ Virchow’s Archiv,” Bd. cxvn. 153. Panum, “ Experimented Beitrage zur Lehre von der Embolie,” “Vir- chow’s Archiv,” Bd. xxv, 1862. 154. Pariser, “ Die Behandlung des frei in die Bauchhohle perforierten Ulcus ventriculi,” “ Allg. medic. Centralz.,” 1896. 155. Pauly, “Zur Lehre vom traumatischen Magengeschwiir,” “ Aerztl. Sachverst.-Ztg.,” No. 2, 1898. 156. Pavy, “On Gastric Erosion,” “Guy’s Hospital Reports,” vol. xiv, 1868. 1 57. Petruschky, J., “ Zur. Diag. u. Therap. d. Primar. Ulcus ventric. tubercu- losum,” “ Verhandlung d. XVII. Congress, f. innere Medicin,” 1899, S. 366. 158. Pfuhl, “ Berliner klin. Wochenschr.,” 1877, p. 57. 159. Potain, “ Ulcere Simple Duodenal et Ulcere Simple de l’Estomac,” “ Bull, med.,” 1, 1, 1897. 160. Poulain, “ Du role del’Infection dans la Pathogenie de l’Ulcere rond,” “ These de Paris,” 1897. 161. Qaife, F. H., “ An Interesting Case of Gastric Ulcer,” “ Australas. Med. Gaz.,” 1898, xvii. 162. Quincke, “ Die Entstehung des Magengeschwiirs,” “ Deutsche med. Wochenschr.,” 1882. 163. Quincke und Daettwyler, “ Correspondenzbl. f. Schweizer Aerzte,” 1875, p. 101. 164. Rabe et Rey, “ Double Ulcere de l’Estomac ; Ulceration du foie et du Pancreas, Retraction Cicatricielle Intense, avec Biloculation de l’Estomac ; Abcess sus-hepato-phrenique, Epanchement Pleuritique Double, Purulent a Gauche, Sereux a Droite,” “ Bull. Soc. Anat. de Par.,” 1897, lxxii. 165. Rasmussen, “Ueber die Magenschwiirfurche und die Ursache des chronischen Magengeschwiirs,” “ Centralblatt fur die med. Wissenschaften,” 1887. 166. Ratjen, “ Ulcus ventriculi, ausschliesslich mit Rectal-Ernahrung be- handelt,” “ Deutsche med. Wochenschr.,” No. 52, 1897. 167. Reichel, “Zur Lehre vom traumatischen Magengeschwiir,” “Aerztl. Sachverst. Ztg.,” Nr. 6, 1898. 168. Riegel, F., “ Zeitschr. f. klin. Med.,” Bd. xn, S. 434, and “ Deutsche med. Wochenschr.,” 1886, Nr. 52. 169. Rindfleisch, “ Lehrbuch der patholog. Anatomie.” 524 ULCER OF THE STOMACH. 170. Ritter, “ Ueber den Einfluss von Traumen auf die Entstehung des Magengeschwiirs,” “ Zeitschr. f. klin. Med.,” xii. 1 7 1 . Rivet, “ Perforation par ulcere de l’estomac,” “ Soc. med. de Nantes,” 10 Dec.; “ Gaz. med. de Nantes,” 1897. 172. Rokitansky, “ Lehrbuch der patholog. Anatomie.” 173. Rolleston, H. D., “ A Case of Latent Ulcer of the Pylorus with Jaun- dice, Simulating Malignant Disease,” “ Practit.,” London, 1897, Liv, 465- 470. 174. Rommelaere, “ Ulcere rond phagedenique de l’estomac deux lesions, une cicatrice a fond pancreatique et un ulcere perforant en activite bouche pir un cartilage costal, sclerose de la parvi prepylorique ; mort, autopsie,” “ Clinique Brux.,” 1897, xi, 521-529. 175. Rosenheim, Th., “ Pathologie und Therapie der Krankheiten der Speiserohre und des Magens,” Wien und Leipzig, 1891, S. 161. 176. Rosenheim, Th., “ Zur Kenntniss des mit Krebs complicirten runden Magengeschwiirs,” “ Zeitschr. f. klin. Med.,” Bd. xvii, S. 116. 177. Rosenheim, Th., “ Deutsche med. Wochenschr.,” 1890, Nr. 15. 178. Rosenheim, “ Die neueren Behandlungsmethoden des Magens,” “ Ber- liner Klinik,” May, 1894. 179. Roughton, E. W., “Perforating Gastric Ulcer; Operation, Death; Necropsy,” “ Brit. Med. Jour.,” July 9, 1898. 180. Sansoni, L., “ II sottonit rato di bismuto ad alte dosi nella cura del l’ulcera semplice dello stomaco,” “ Gior. d. r. accad. di med di Torino,” 1897, 3 s., xlv, 463-468. 181. Saundby, “ Ein Fall von sanduhrformiger Einschniirung des Magens in Verbindung mit einem kolossalen Magengeschwiir,” “ Deutsche med. Wochenschr.,” 1891. 182. Savelieff, “ Ueber die Wismuthbehandlung des runden Magenge- schwiirs,” “ Therap. Monatshefte,” 1894, Nr. 10. 183. Scheel, V., “ Et Tifaelde af Ulcus ventriculi,” “ Hosp.-Tid. Kjobenh.,” 1898, 4. R., vi. 184. Scheurmann, “Ueber die Haufigkeit des runden Magengeschwiirs in Miinchen,” Dissert., Miinch., 1895-96. 185. Schiff, “ Beitrag zur Kenntniss des motorischen Einflusses der in Seh- hiigel vereinigten Gebilde,” “ Arch. f. physiol. Heilkunde,” v, 1846. 186. Schiff, “ Ueber die Gefassnerven des Magens,” ibid., xm, 1854, S. 30. 187. Schmidt, “ Anatomische Beitrage zur Genese des Ulcus ventriculi,” Dissert., Leipzig, 1895-96. 188. Schiitz, R., “ Differential Diagnose d. UlcuS Ventriculi,” ibid., S. 417. 189. Sehrwald, “ Was verhindert die Selbstverdauung des lebenden Magens ? Ein Beitrag zur Aetiologie des runden Magengeschwiirs,’-’ “Miinch. med. Wochenschr.,” 1888. 190. Shaw, G. F., “ Hematemesis as a Sequence of Chronic Ulcer,” “ Med. Rec.,” New York, 1898, liv, 138. 191. Silbermann, “ Deutsche med. Wochenschr.,” 1886, Nr. 29. 192. Sohlern, V., “ Der Einfluss der Ernahrung auf die Entstehung des Magengeschwiirs,” “ Berl. klin. Wochenschr.,” 1889, Nr. 14. 193. Stawell, R. de S., “ Perforating Gastric Ulcer,” “ St. Barth. Hosp. Jour.,” London, 1897-98, v. LITERATURE ON ULCER OF THE STOMACH. 525 194. Stepp, “ Zur Behandlung des chronischen Magengeschwiirs,” “ Ver- handlungen der 65. Versammlung deutscher Naturforscher und Aerzte,” 1893. 195. Sticker, “ Ueber den Einfluss der Magensaftabsonderung auf den Chlorgehalt des Harns,” “ Berl. klin. Wochenschr.,” 1887. 196. Sticker und Hubner, “ Wechselbeziehungen zwischen Secreten und Excreten,” “ Zeitschr. f. klin. Med.,” xil, 1887. 197. Stockton, Chas. G., “ The Etiology of Gastric Ulcer,” “ Med. News,” Jan. 14, 1893. 198. Sutherland, L. R., “ A Series of Specimens of Perforating Ulcer of the Stomach and Duodenum,” “ Glasgow Med. Jour.,” 1898, XLIX, 207-215. 199. Talma, “ Untersuchungen iiber Ulc. ventr. simpl. Gastromalacie und Ileus,” “ Zeitschr. f. klin. Med.,” xvn, 1890. 200. Taylor, S., “ Gastric Ulcer,” “ Med. Press and Circ.,” London, 1898. n. s., LXV, 297-300. 201. Thorspecken, “ Ein Fall von Magenerweichung ante mortem,” “ Deutsches Arch. f. klin. Med.,” xxxm. 202. Tournier, C., “ D’un type cle catarrhe gastrique avec hyperesthesie de la muqueuse et colite mucomembraneuse ; difficultes diagnostiques avec l’ulcere,” “ Province med.,” Lyon, 1898, xil, 457-461. 203. Troisfontaines, “ Ulcere simple de l’estomac, chez une jeune homme ; mort; examen anatomique,” “Ann. de la Soc. de med. de Liege,” Juin, 1896, 204. Tuffier, “ Epaississement des parois stomacales du a un ulcere prob- able,” “ Soc. de Chir.,” 27 Oct., 1897. 205. Uhlrich, Chr., “ Sequelae ulceris ventriculi perforati,” “ Biblioth. for Laeger,” p. 367. 206. Vasilin, C., “ Ulcerul simpiu al stomac uli si tratamentul Boas,” “ Spitalul,” Bucuresci, 1898, xvn. 207. Virchow, R., “ Virchow’s Archiv,” Bd. V, p. 363. 208. Von Leube und Mikulicz, “ Chirurgische Behandlung des Magenge- schwiirs,” Abstr. “ Deutsche med. Wochenschr.,” 1897, xxm, Ver. Beil., 83. 209. Warren, J. C., “ The Surgery of Gastric Ulcer, with the Report of a Case of Gastrolysis,” “ Boston Med. and Surg. Jour.,” Sept. 29, 1898. 210. Weir, Robt. F., and E. M. Foote, “ The Surgical Treatment of Round Ulcer of the Stomach and Its Sequelae, with an Account of a Case Successfully Treated by Laparotomy,” “ Med. News,” April 25 and May 2, 1896. 21 1. Welch, cited from Osier’s “ Practice of Medicine,” p. 369. 212. Welti, “ Drei Falle von Verbrennungstod,” “ Centralblatt fur allg. Path.,” 1890. 213. Widal et Meslay, “ Ulcere rond developpe au cours dune pyhemie a staphylocoques ; de lorigine infectieuse de certains ulceres ronds perforants de l’estomac,” “ Bull, et mem. Soc. med. d. hop. de Par.,” 1897, 3 s., xiv, pp. 379 - 385 - 214. Winternitz, W., “ Die Hydrotherapie des Ulcus rotundum ventriculi,” “ Deutsche med. Wochenschr.,” Nr. 46, 1897. 215. Wynter, W. E., “ On Gastric Ulcer Treatment,” London, 1897, 1, 462- 464. 216. Ziemssen, “Ueber die Behandlung des einfachen Magengeschwiirs,” “Volkmann’s Sammlung klinischer Vortrage,” 1871, Nr. 15. 526 ULCER OF THE STOMACH. We refer also to “ Literature on Gastric Ulcer” in Prof. William H. Welch’s article in “American System of Medicine,” vol. ir, p. 480, in which over 140 important bibliographical references are given. In the fourth volume of Penzoldt and Stintzing’s “ Handbuch d. speciellen Therapie,” vol. iv, pp. 316, 317, also pp. 437 and 438, are contained 150 biblio- graphical references on the treatment of Gastric Ulcer. BIBLIOGRAPHY OF ULCUS CARCINOMATOSUM. 1. Berthold, Inaug.-Dissert., Berlin, 1883. 2. Biach, “Wien. med. Presse,” 1890, Nr. 3. 3. Boas, “ Diagnostik u. Therapie d. Magenkrankh.,” p. 8. 4. Bouveret, “ Traite de malad. d. l’estomac,” Paris, 1893, p. 274 (three cases). 5. Brinton, “ Lectures on Diseases of the Stomach,” London, 1864. 6. Dittrich, “ Prager Vierteljahresschrift,” v, 1848, S. 1. 7. Eisenlohr, “ Deutsche med. Wochenschr., ’ 1890, Nr. 52. . 8. Ewald, “ Klinik d. Verdauungskrankh.,” 1885. 9. Feiertag, Inaug.-Dissert., Dorpat, 1894. 10. Hauser, “ Das chronische Magengeschwur,” Leipzig, 1883. 11. Heitler, “Wien. med. Wochenschr.,” 1883, Nr. 31. 12. Koch, R., “ St. Petersburger med. Wochenschr.,” 1893, Nr. 43. 13. Kollmann, “ Zur Differentialdiagnose zwischen Magengeschwur und Magenkrebs,” 1891, Nr. 5, 6. 14. Krukenberg, Inaug.-Dissert., Heidelberg, 1888. 15. Kulcke, Inaug.-Dissert., Berlin, 1889. 16. Langguth, “ Archiv f. Verdauungskrankh.,” von Boas, Bd. 1, S. 355, “ On Significance of Lactic Acid.” 17. Lebert, “ Die Krankheiten d. Magens,” Tubingen, 1878, S. 440. 18. Leube, “ Ziemssen’s Handbuch,” Bd. vii, S. 124. 19. Meyer, C., Inaug.-Dissert., Heidelberg, 1885. 20. Oppler und Boas, “ Zur Kenntniss d. Mageninhalts b. Carcinome,” etc., “ Deutsche med. Wochenschr.,” 1895, Nr. 5. 21. Pignal, “ These de Lyon,” 1891 (two cases). 22. Plange, Inaug.-Dissert., Berlin, 1859. 23. Riegel, F., “ Die Erkrankungen d. Magens,” p. 174. (On the Oppler- Boas bacillus.) 24. Rokitansky, “ Lehrbuch d. patholog. Anatomie,” third edition. 25. Rosenheim, “ Zur Kenntniss des mit Krebs complicirten runden Magen- geschwurs,” “ Zeitschr. f. klin. Med.,” Bd. xvii, S. 116. 26. Schlesinger und Kaufmann, “Wien. klin. Rundschau,” 1895, Nr. 15. (On the Oppler-Boas bacillus.) 27. Steiner, Inaug.-Dissert., Berlin, 1868. 28. Sticker, “ Verhandl. d. Congresses f. innere Med.,” 1887. 29. Tapret, “Union medic.,” 1891, No. 98. 30. Thiersch, “Munch, med. Wochenschr.,” 1886, Nr. 13. 31. Waltzold, “ Charite-Annalen,” Bd. xiv. 32. Wollmann, Inaug.-Dissert., 1868. CARCINOMATA. 527 CHAPTER IV. MALIGNANT TUMORS OF THE STOMACH. (A) CARCINOMATA. Pathology. — In accordance with leading pathologists we may distinguish four types: 1. The cylindrical cell, or adenocarcinoma. 2. The soft glandular, or medullary carcinoma. 3. The hard glandular carcinoma, or scirrhus. 4. The mucous, or colloid carcinoma. In the section on the Surgical Operations on the Stomach we have spoken of the relative frequency with which these various types of carcinoma attack this organ. It is an error for clinicians to speak of gastric cancer as if this were the only type of malig- nant neoplasm that can attack the stomach. Inasmuch as these various types show different rates of mortality after operation, and as they can occasionally be distinguished clinically by small bits of the new growth, which come up in the wash-water or are found caught in the eyes of the stomach-tube, it is essential that a brief pathological description of them should be given. The types which we have mentioned are not sharply distinguished from each other, but many gradations and transitions exist between them. The structure of a gastric malignant neoplasm is by no means a matter of indifference, both for the clinical history and the pros- pective surgical treatment. The scirrhus exhibits the most pro- tracted course ; the medullary (soft glandular) a disposition to disintegration and formation of metastases ; while the colloid has a tendency to extend to the peritoneum, and rarely forms metastases. The cylindrical cell, or adenocarcinoma , presents a soft, distinct prominence, or tumor, upon the surface of which smaller fungoid elevations develop, being attached to the fundamental tumor by broad or narrow bases, which give the surface a papillary appear- ance. In this case the tumor regularly has a red color, because each individual fungosity contains a small loop of blood-vessels. The little vessels in the outer, as well as those in the inner, sections of the neoplasm frequently show an irregular spindle-shaped or spherical dilatation, so that this form of carcinoma has been called by Orth, telangiectatic. This condition of the blood-vessels may 528 MALIGNANT TUMORS OF THE STOMACH. explain why, in this type of cancer, smaller or larger extravasations of blood are found on the surface, as well as in the parenchyma ; and also accounts for the frequent effusion of blood into the cavity Fig. 35. — Cancerous Invasion of the Glandular Layer. A Portion of the Mucous Coat. — ( From the Author's Clinic.') Objective, one-sixth. Eyepiece, one inch. X about 320 diameters. Stained with hematoxylin and orange G. This cut shows very well the small, round-cell infiltration between the cross-sections of the gastric tubules, with here and there the cells very much crowded, A, A. The exfoliation of the cells lining some of the glandular acini is also shown in places, B. At one or two places the proliferation of the epithelial cells that line the glands, with breaking of these glandular structures and the escape of some of the cells into the surrounding tissue, is seen, C, C, C. The entire obliteration of some of the glandular structures by masses of cancer cells, Z), D, which in many places are strung out for some distance, E, E, and in a few others have taken on the pseudo-glandular arrangement, E, is also well shown. of the stomach. On section, the so-called “ carcinoma juice ” ap- pears abundantly on the surface, and in this “juice” typical cylin- drical cells are generally exclusively found in sections examined ADENOCARCINOMA OF THE STOMACH. 529 microscopically. Such sections present varying pictures, accord- ing to whether they are taken from the surface or from deeper regions of the neoplasm. On the surface the aspect closely re- sembles that of a papillary fibroma, but in the deeper regions a C Fig. 36.— Cancerous Infiltration of the Muscularis. Section of a Portion of the Muscular Coat of the Stomach. — ( From the Author's Clinic .) Objective, one-sixth. Eyepiece, one inch. Stain, hematoxylin and orange G. X about 320 diameters. Cross-section of bundles of muscle-fibers from the muscular coat are shown, A, between which there are a large number of small round cells, B, B, in places, and here and there large clumps of cancer cells, C, C , C, C, a few of which show the attempt at pseudo-glandular formation, D , Z>, in some instances arranging themselves in complete circles, while in others only a portion of an acinus is formed. glandular structure becomes very distinct, for here cylindrical cells may be seen lining tubular, hollow spaces in a regular manner, these tubular ducts being separated by connective tissue, which 35 530 MALIGNANT TUMORS OF THE STOMACH. generally shows small-celled infiltration ; nor are these glandular hollow spaces always regular in distribution or in size. The order of the lining cell is, in so far, a typical one, as the whole cavity is filled with cells of which only the outer ones are cylindrical and arranged in regular order, while the rest show very irregular re- lations, both in form and position. The cylindrical cell carcinoma is most frequently found in the pyloric region, its favorite place being close to the valve, and generally sharply limited toward the duodenum. It is probable that the neoplasm originates here from the pyloric glands, while at other locations of the stomach the sur- face epithelium and the cylindrical cells of the gland vestibules form -the bases of origin. The papillary forms of these cancers particularly have a tendency to grow toward the surface, for they may last a long time ; i. e ., the cancer mass may assume a con- siderable size before the infiltration will invade the outer layers of the stomach wall. The development of secondary carcinomata may also take a long time, so that with very large malignant neoplasms perhaps only one or a few lymph glands will be found secondarily involved. Finally, ulcerations of the surface may pro long development ; or, if a loss of substance does occur, it may be compensated for by proliferation of the tumor tissue ; eventually, however, with the co-operation of necrosis, a larger destruction occurs. The ulceration is usually surrounded by a projecting fungus-like wall. Occasionally the ensuing necrosis — which presumably arises from disturbances in the circulation — may become so extensive that the entire tumor, with the exception of very few remnants, •may be sloughed off, leaving behind an ulcerating base. The break- down and destruction of the tumor mass frequently progresses in a gangrenous manner, and then we may find not only formations of cavities within the tumor, but the entire stomach walls may also be perforated, while large cancerous proliferations are still left close to the perforation. The second main type, the soft glandular or medidlary car- cinoma, likewise forms knotty projections on the inner surface of the stomach, but it is very rare that these are observed intact; on the contrary, this type of cancer usually appears at the necropsy as a cancerous ulceration. Its form is quite characteristic. It pre- sents a navel-like, deepened center and an external surrounding wall which is formed by the mass of the tumor; it is either broad or narrow, high or low; at times it exhibits a uniform appear- ADENOCARCINOMA OF THE STOMACH. 531 ance ; again, it is irregularly ragged in outline. In the bowl-shaped central depression the tumor mass is found breaking down in fragments, or, occasionally, this depression may be found smooth, since the more resistant muscularis may have been exposed and is, Fig. 37. — A Portion of an Area in the Submucosa, Largely Composed of Groups of Cancer Cells. — ( From Author's Clinic .) Objective, one-sixth. Eyepiece, one inch. Stained with hematoxylin and orange G. X about 320 diameters. The fibrous tissue of the mucosa is infiltrated with many small round cells, which in some places are very numerous, A , A. The most prominent change appears in the numerous clumps of cancer cells, most all of which lie in open spaces in the tissue, B. These clumps are like those seen in other coats of the stomach, but the attempt at glandular formation is more marked here than in any other locality, C, C. In the upper part of the cut is seen the lower portion of the mus- cularis mucosae, D, D, infiltrated with many small round cells, and containing a few of the masses of cancer cells. presumably, destroyed much more slowly than the other layers by the action of the gastric juice. In this tumor also the destruction may go on to complete perforation of the gastric wall. The masses 532 MALIGNANT TUMORS OF THE STOMACH. of the tumor which surround the ulceration denote more or less ex- tensive retrogressive metamorphoses, accompanied by hemorrhages, and, not rarely, an ichorous deterioration of the tumor mass. On microscopical examination of these masses, it is noticed that the cancer cells are, as a rule, quite small and irregularly shaped, simi- lar to oxyntic cells, but that their numbers far exceed the stroma, Fig. 38. — Section of Tissue Near the Base of a Carcinomatous Ulcer, Showing Micro- organisms. — ( From Author's Clinic.) Objective, one-twelfth. Eyepiece, one inch. Stained with methyl-violet, anilin-oil solution by Gram’s method. X 1060 diapieters. a , a , a. The Oppler-Boas bacillus, singly and in chains. The peculiar base-ball bat shape is shown in some cases, while in others it is seen that one end of the rod is narrow and the other broad, the change in size being sudden. Some of the rods stain solidly, while in others there are clear spaces. b, b, b. A micrococcus which occurs singly and in clumps, but never in chains. These, as well as the Oppler-Boas bacillus and the next organism to be described, were found both in the necrotic tissue over the base of the ulcer and in the healthy tissue below the same. c, c, c. A peculiar yeast-like organism, that is probably some protozoan. It is much smaller than a yeast cell. Budding forms are seen, and the granular protoplasm in some, and the few large deeply staining dots in others, are well represented. which in many places consists chiefly of very thin, delicate parti- tions. Larger supporting partitions of the stroma exist, of course, in addition to these, and in this latter type “ small-celled infiltra- tion ” is regularly present. Microscopical examination evinces the fact that the soft glandular cancer rapidly invades the exterior gastric layers, for small nodules (tumor knots) appear at the serosa at an early stage, which nodules distinctly show, and correspond to, MEDULLARY CARCINOMA. 533 the course of the lymphatic vessels. These nodules have arisen by a direct advance of the cancer into and through the muscular layer, in which, microscopically, a distinct thickening is observed, this thickening being dependent upon proliferation of the mus- cular substance itself, as well as upon a broadening of the inter- muscular connective septa. ( Fig. 36.) Examining microscopically a section through the muscularis, it at once becomes evident that the cancer masses, in their invasions between the muscular fibers, follow the septa which conduct the lymphatic vessels. In older cases, small foci are found in the muscle-bundles them- selves, where they have forced apart the muscle cells to assume the shape of spindle-like spaces. As the growth of the carcinoma is much more restricted in the denser and closer netted muscularis than in the subserosa, the cancer masses outside of the muscular layer are generally considerably more voluminous than those within it. The (soft) medullary carcinoma may extend toward the surface as well as toward the interior, and it will then be seen that it habitually follows preformed passages — namely, along the peri- lymphatic spaces. In very rare cases this neoplasm may extend over the whole stomach, except, possibly, the fundus; and in such a case Orth has found that the entire lymphatic network of the mucosa, as well as of the submucosa, was filled with cancerous masses. The greater tendency of the medullary carcinoma for local dissemination corresponds to its relations toward the general organism. With this neoplasm particularly, one finds extensive lymphatic gland carcinomata, not only in the epigastric, celiac, portal, and retroperitoneal, but also very frequently in the left supraclavicular lymph-glands ; one may find metastases in the lymph- as well as in the blood-channels, and, besides, a dissemina- tion of cancerous nodules in the abdominal cavity. Concerning the seat of medullary cancers, it may be said that they are not limited to any particular part of the stomach, for they may be found at the cardia, the anterior and posterior walls, and the lesser curvature as well as in the pyloric region, for which they have an unmistakable affinity. Frequently, cancers of the cardia extend to the esophagus, while the duodenum remains intact. The scirrhus (meaning hard glandular) is distinguished from the two preceding types of carcinoma mainly by its hardness. It pro- duces no large tumor nodules, but rather simple thickenings of the entire wall. The surface of the mucosa shows, as a rule, a flat ulcer- ation, which has either a smooth or an actually cicatricial basis, or 534 MALIGNANT TUMORS OF THE STOMACH. else a papillomatous, irregular, and corroded appearance. The edges of the ulcerations are generally entirely flat, without a trace of the wall-like elevation, and for that reason the transition into the sur- rounding mucosa is very gradual. On cutting through a scirrhous gastric wall considerable resistance is met with, so that the tissue actually grates on cutting. Microscopical section reveals a thickening of all layers, particularly of the muscularis, by a gray- ish-white, striated, cicatricial connective tissue. Typical cancer- ous proliferation is not apparent on the mucosa nor in the remain- ing layers of the gastric wall, so that it may be doubtful whether one is dealing with a cancer or with a simple chronic ulcer. To decide this question one must observe the relation of other parts, and, particularly, search for secondary cancer formation. As a matter of fact, one occasionally sees small, flat tumor nodules on the serosa directly over the neoplasm ; but as exten- sive adhesions of the pylorus with neighboring organs (liver, intes- tine, omentum) are invariably present with this form of cancer, implicating the peritoneum, such nodules are difficult to recognize, even if they are present. A more reliable sign is the condition of the lymphatic glands, which usually show cancer formation ; and, besides this, the liver and other organs, which are otherwise rarely invaded (for instance, the spinal column), may be found to contain it. Such cases easily give rise to deception, because these second- ary tumors may show a medullary structure and attain con- siderable size, in which case the seemingly unimportant scirrhous ulceration in the stomach may be overlooked. The surest indica- tion of the character of these changes is obtained from microscop- ical examination, though in a section-preparation hardly anything else but fibrous connective tissue is seen, particularly in the very much thickened muscularis, which is permeated with broad, gray- ish-white stripes. But when a larger number of preparations are carefully examined the histological peculiarities of carcinoma, the connective-tissue stroma, and carcinoma bodies are discovered. The last-named are diminutive and consist of small-celled rows. The stroma is massive, and composed of tough, rigidly fibered con- nective tissue. The longitudinal direction of the small cell-rows is parallel to the course of the fibers of the stroma. It is noteworthy that the secondary cancer nodules of scirrhus are richer in cells, and therefore more closely resemble the medullary carcinoma; and also that, alongside entirely fibrous places in the gastric wall, here and there at the edges of the ulcerations places can be found THE GASTRIC SCIRRHUS. 535 where the cancer cells are not as yet so scarce in proportion to the stroma, and where the latter does not as yet possess the character- istic callous consistency. It may, from this, be concluded that the scirrhus is, in fact, an atrophic cancer ( cancer atrophicans) — i. e. } that the callous formation represents nothing more than a later stage, or result, of the initial cancerous process. The question has arisen whether complete healing may not be produced by a total callous metamorphosis of the neoplasm ; but, up to the present time, no convincing observations confirmatory of this question have been made. It is reasonable to assume that a very localized callous cicatricial healing may be brought about in certain places, while in other portions (the very youngest parts of the neoplasm) very slow but gradual cancerous progress is made. The callous stroma of the scirrhus has a tendency to contract such formations. This fact is of great significance, when the microscopical rela- tion of the scirrhus is considered, for it explains the stenosis which it causes at the pylorus, — its almost exclusive locality. This constriction is further increased by the very much thickened and callus-like alteration of the gastric wall, which becomes unresis- tant and inelastic, resembling a hard rigid ring, or stiff tube. It is self-evident that a pylorus changed in this manner is no longer capable of closing off the stomach toward the duodenum (incon- tinence of the pylorus). The extent of the scirrhus from the pylorus toward the cardia may be variable, rare cases occurring in which the entire gastric wall is in a state of scirrhous degeneration. The entire organ is then, as a rule, considerably contracted, and at the same time the walls are very much thickened. On the inner surface little mucous membrane remains in these cases. We have seen elsewhere that a similar condition may be brought about by chronic inflammation (hyperplastic gastritis, cirrhosis of the stom- ach). The differential diagnosis is very difficult to establish from the local conditions, but the majority of stomach contractions are to be attributed to scirrhus (Orth, loc. cit.). At any rate, it is well always to think first of all of this neoplasm. The colloid carcinoma in typical cases has a very characteristic appearance. It does not produce circumscribed tumor masses so much as diffuse thickenings of the entire wall similar to scirrhus. In this growth the stroma is not a bright fibrillar tissue, but a gela- tinous, translucent, colorless or light-brown material. These masses are recognizable on the inner surface, which, as a rule, presents an extended flat ulceration. Where the tumor tissue lies 536 MALIGNANT TUMORS OF THE STOMACH. exposed there appears a distinct, alveolar, grayish framework, which incloses the colloid granules, in dimension the size of a pin- head or a millet seed. The whole mass has a slimy, mucoid feeling, but it is not nearly so soft as genuine mucus. Micro- scopically a similar picture obtains ; for here, also, the connective- tissue alveolar framework, containing a transparent mucocolloid mass in its meshes, is prominent. This mass may be entirely devoid of cellular elements, but generally a number of cells and cell fragments are detected, in which it can be distinctly recog- nized that these cells themselves furnish the colloid material of the alveoli, for one frequently sees many cells in a swollen state, either with hyaline granules or in a condition of disintegration. In other places cells may be found in better preservation, while the colloid matter is not so pronounced, so that, in this form of carcinoma, just as in scirrhus, there are transitions to the medullary type. Here, likewise, the youngest portions of the growth are those most rich in cellular elements, and production of colloid material is a phenomenon which occurs in the course of further development of the tumor. “ Colloid tissue ” several centimeters thick may be found through- out the entire gastric wall, and here again the lymph-vessels offer the channels in which the cancerous masses take their course, and in which they ramify both interiorly and superficially. Occasionally, larger colloid tumor nodules may appear on the serosa; and, in fact, the colloid carcinoma not rarely invades the peritoneum and produces an extensive carcinosis — as a result of which the omen- tum is transformed into a short, thick, and board-like band. Af- fections of the lymphatic glands, liver, lungs, and other organs, are by no means absent. The colloid carcinomata also have their favorite location in the pyloric region, whence they may extend to the duodenum, and also to the liver, by direct continuity. The extension to the liver generally occurs after the formation of a previous adhesion. A transition to the esophagus from the cardia has likewise been observed. Although the colloid carcinoma pro- duces no large prominent tumors, it may extend far over the gastric surface, and frequently takes in the entire wall, reducing the size of the stomach somewhat, but not to such a degree as scirrhus. The wall is hard and immovable, the inner surface ulcerated, the outer coarsely granular from small and large cancerous nodules of the peritoneal covering. Although the ulcerations of the colloid carcinoma may have STRUCTURAL EFFECTS OF GASTRIC CANCERS. 537 considerable superficial extent, still a perforation rarely results, although the ulcerations may, at places, reach even to the perito- neum. The colloid tissue is not subject to rapid disintegration, hence new tumor masses may be formed in front of the basis of ulceration. Structural Effects of Malignant Gastric Neoplasms. — The development of gastric carcinoma is accompanied by adhesions of the serosa with the pancreas, liver, the transverse colon, the anterior abdominal wall, and the omentum ; and, at the same time, there occurs a callous hyperplasia of all connective tissue in the immediate neigh- borhood. The result is that the stomach, particularly the part most frequently affected (namely, the pylorus), becomes fixed, while in other rare cases such adhesions may not be formed, and the stomach is dislocated downward by the tumor masses, in which case the pylorus may extend as far as the symphysis pubis. Fre- quently the cancerous stomach exhibits changes of size and form. We may have diminutions in size accompanying the total degen- erations of stenosing cardiac carcinomata, or, what is more common, dilatation accompanied by marked muscular hypertrophy. The dilatations originate from the obstruction of the passage through the pylorus, a pyloric stenosis existing. This may be caused by a variety of circumstances. Among the causes so operating may be mentioned, in the first place, a large tumor mass located in the pyloric orifice, acting like a cork or ball-valve ; secondly, the rig- idity which the walls undergo in scirrhus and in colloid carcinoma; finally, the effective contractions of the scirrhus, whereby a consid- erable resistance is offered against the advance of the gastric con- tents. These disturbances may be increased by a large variety of inflections and dislocations resulting from adhesions, as well as by the weight of the accumulating gastric contents. Incontinence of the pylorus may occur contemporaneously with stenosis, but it may also exist in a very severe degree without stenosis where the cancerous ulceration has destroyed more or less of the pyloric ring. These changes at the pylorus are important because they are very frequent, for, as is evident from what we have said concerning the various types of carcinoma, the pyloric antrum is the most frequent seat of cancer formation. According to the statistics of William H. Welch (“ A System of Practical Medicine by American Authors,” edited by William Pepper, vol. n, p. 561), the frequency of carcino- mata occurring at the pyloric region is 60.8 per cent. ; at the lesser curvature, 1 1.4 per cent. ; at the cardia, 8 per cent. ; at the posterior 538 MALIGNANT TUMORS OF THE STOMACH. wall, 5.2 per cent.; the whole, or the greater part of the stomach, 4.7 per cent. According to Orth, 60 per cent, of all gastric cancers invade the pylorus; 20 per cent., the lesser curvature; 10 per cent., the cardia ; and the rest, the remaining parts of the stomach. As gastric carcinoma makes up 35 to 45 per cent, of all carcinomata, the great importance of pyloric cancer can be appreciated. In the midregions of the stomach the cancers are limited to a portion of the circumference, but in the vicinity of the two openings they fre- quently occupy the entire circumference in a ring- or girdle-shaped manner. The growth of carcinomata occurs partly through simple periph- eral extension, partly through daughter nodules which develop at some distance from the main tumor, but sooner or later coalesce with it. These nodules evidently lie underneath the mucosa, which may be movable over them ; hence, it may be assumed that they have arisen through infection by way of the lymph-channels. The frequent occupation of lymphatic vessels by cancer masses in the neighborhood of larger nodules argues in favor of this view. Concerning the secondary infection of lymph-glands, it may be stated that, with gastric carcinomata, it often happens that glands are diseased which do not receive their lymph from the direction of the stomach ; for instance, the retroperitoneal. It is possi- ble that this is caused by the cancerous impermeability of glands located higher up, which compels a return of the lymph-current. Following the current of the lymph, it has been found, by Orth and others, that the thoracic duct may be infected. Possibly, the infection of the left supraclavicular lymph-glands occurs in con- nection with the transportation of cancer-cells through the lymph of the thoracic duct. The lymph-vessels of the diaphragm may be entirely filled with cancerous masses, and may disseminate the ele- ments of the disease to the pleural cavity, bronchial glands, and lungs. The author has studied sections obtained by operation during attempts to execute a Heinecke-Mikulicz pyloroplastic operation from two cases of what proved to be gastric scirrhus later on. In neither case did microscopical examination reveal any foci of cancer cells ; a large number of sections were examined, and the appearance was that of a chronic hyperplastic gastritis. Nowhere could any small cell rows of cancer bodies be discovered in the dense connective-tissue stroma. Later on, metastases developed, which gkve evidence of the malignant nature of the original gastric induration. This experience has led the author to STRUCTURAL EFFECTS OF GASTRIC CANCERS. 539 urge gastroenterostomy, or, if possible, resection in all doubtful cases of chronic hyperplastic gastritis. If it should happen that a simple benign but hyperplastic gastritis is treated in this way, the patient will be the gainer by the operation, for this form of gastritis is as fatal as the malignant types, owing to the absolute rigidity of the stomach and loss of peristalsis which it produces. In twenty-five per cent, of all gastric cancers secondary nodules are contained in the liver. The infection being transported by direct extension after “adhesive invasion,” by the lymph-current from the porta hepatica or transportation by the blood-stream, the latter mode being by far the more plausible. The metastases may occur through minute particles that are not retained emboli ; whereas, in other instances, emboli can be demonstrated in the larger ves- sels, proving that such emboli can originate from the stomach, because the gastric veins are roots of the portal vein, and cancer- ous invasion of the veins of the stomach is conceded. The spread- ing of gastric cancer to the esophagus, duodenum, spleen, pancreas, and intestines occurs by direct extension along the paths that are either normally present or newly formed pathologically. Participa- tion of the peritoneum has its foundation in the direct extension of the carcinoma into the gastric serosa ; when, however, the peri- toneum is once invaded, the rest of it is not affected by continued simple extension of the growth, although this may occur with col- loid carcinomata, but by dissemination, which means the falling of tiny particles into the peritoneal cavity (carcinoma seed, as it were) and their attachment in suitable places (at first in the deepest por- tions of the peritoneum, in the rectovesical and rectouterine pouch). It is evident that gravity is an element in the spreading of peritoneal carcinoma. The ulcerations of gastric cancers depend partly upon ichorous degeneration and suppuration and partly upon the digest- ive influence of the gastric juice, which occasionally causes perfora- tion of the stomach. The vessels of the stomach and of the spleen may be affected by an inflammatory gangrenous ulceration, which may lead to dangerous hemorrhages, but these cases are infrequent. Cancerous ulcerations are very similar to the simple peptic ulcer, from which they may be distinguished only by the presence of the tumor wall, which, if absent, enhances the difficulty of distinction between the two. If, indeed, cancer masses are found in the sur- roundings of such an ulceration, the questions may be asked, Has the ulceration arisen from a carcinoma, or Has a simple gastric ulcer been secondarily affected by cancer transformation? Here 540 MALIGNANT TUMORS OF THE STOMACH. the clinical history, as well as the examination and analysis of gas- tric contents, may give the desired information. Rosenheim has shown that normal or supernormal hydrochloric acid secretion persists in the carcinoma which has secondarily developed from an ulcer ; but when the carcinoma is the primary growth, the hydro- chloric acid is permanently absent at an early stage in the disease. Anatomically, it may be stated that when the ulceration has a regular bowl-shaped appearance, and is on every side surrounded by tumor masses, even where no cancer masses can be found in its base, the carcinomatous tumor was undoubtedly the primary, the ulceration the secondary, object; and, reversely, when a simple ulcer, accompanied by all typical peculiarities, presents a thicken- ing only at one side, the latter tumor mass must be regarded as secondary and the ulcer as primary. The remaining gastric mucous membrane sometimes shows insignificant alterations, which agrees with clinical observations as to gastric cancers remaining latent. In other cases a pronounced chronic inflammation is pres- ent, particularly in the immediate vicinity of the tumor masses or ulcerations. A hypertrophy of the musculature is frequently apparent, which partly depends upon alterations in the mucosa and partly upon a pyloric stenosis, the latter being responsible for the condition of the gastric contents, because it provokes dilatation and its consequences. The loss of secretion and the admixture of blood with the gastric contents is directly traceable to the cancer- ous infiltration or the accompanying gastritis, or both. The hemor- rhages may arise by ulcerative disintegration, as well as from rupture of the small vessels in the villous cancer proliferations. What is the source or basis of the primary development of can- cer formation ? According to prevalent views, all gastric carcino- mata do not originate from the connective tissue of the submucosa, as was formerly believed, but from the mucosa, and particularly from the glandular, or surface, epithelium of the same, the cells of these carcinomata having great similarity to the various cells of the mucosa. All gastric carcinomata are therefore epithelial tumors. We owe to Waldeyer the first exact investigations concerning the beginning of cancer formation, which have been confirmed later by other researches. According to him, the process begins with an enlargement and hypertrophy of a group of ten or twelve glands, which, breaking through the muscularis mucosae, enter the sub- mucosa. The cells of these gland-ducts react differently to stain- ing reagents, being colored much deeper, and filling the lumen ORIGIN OF GASTRIC CANCER. 541 of the gland in an irregular manner. A further step is that the connective tissue of the mucosa, and particularly of the submucosa, undergoing a transformation into granulation tissue, advances and is pushed up against the aggregations of epithelial cells, which are thus forced apart and inclosed in groups by the connective tissue, giving rise to the cancer alveoli and cancer bodies (cancer cells). Accepting this as a general rule, the question arises, What causes this gland group and the adjoining connective tissue to enter upon this abnormal growth ? Cohnheim says that abnormal conditions of primitive germinal tissue are present here, a remnant of unused primitive cells from which the proliferation starts. This is a hypothesis which can admit of no proof, since after the prolifera- tion has occurred it is impossible to obtain any knowledge of the condition of the locality that existed there prior to the prolifera- tion. But even admitting Cohnheim’s theory, we must ask, Why do these embryonic cells suddenly begin to grow after many years? There must evidently be some other incentives to growth. There is undoubtedly some disposition toward the development of gastric cancers with advancing age. What the nature of this predisposition is we do not know. There seems to be no predis- position of sex, for both sexes are attacked with equal frequency. The pronounced tendency which the structures of the pylorus ex- hibit toward cancerous infection attracts attention to the mechani- cal relations there existing. Hauser has made some interesting observations on the development of cancers from simple peptic ulcers. He has shown that the gastric secretory glands at the edges of healing ulcers undergo a proliferation which may be augmented to a cancerous neoplasm, and he seeks the explanation for this process in an increased supply of nutritive material to the glands, and in a reduction of the resistance of the adjoining tissues in consequence of an ulcerative and cicatricial process. As frequent as primary carcinomata are, just so rare are the secondary. Secondary cancers may arise in the stomach by direct extension from the immediate surroundings. In this manner a cancer might extend to the gastric walls from the pancreas, liver, and lymphatic glands. Clinically, the most important of the primary carcinomata is the esophageal, which, when it is located at the car- dia, may invade the stomach. Reversely, the extension of gastric cancer into the esophagus is really more frequent. There is another kind of extension of esophageal, lingual, and facial carcinomata to the stomach, which is not transmitted by the lymph- or blood- 542 MALIGNANT TUMORS OF THE STOMACH. channels, but by a direct implantation of cancer cells upon the mucosa. Klebs was the first to report three of such cases, and Beck has investigated a case, concerning which he assumes, on the strength of his microscopical preparations, that the loosened parts of the esophageal cancer had fastened themselves in the gastric glands. The new nodules which were thus formed were flattened epithelium carcinomata, composed of the typical pavement-epithe- lium of the esophagus. This raises the interesting question whether the new tumors arise solely and exclusively from the im- planted tumor cells, or whether these cells produce a kind of infec- tion of the local cells upon which they fall, so that the latter are converted into pavement-epithelium cancer cells. Klebs assumes the latter view, but Beck leaves the question undecided. In the place occupied by the tumor that he investigated, no gastric cells were observable, and also no transition forms to pavement cells. The secondary cancers of the peritoneum, already described, arise in a similar manner — namely, by the falling of cancer particles into the peritoneal cavity. Reversely, it has been observed that an implantation carcinoma may arise upon the gastric serosa from a deeper portion of the abdominal cavity. Orth describes a case in which the inner mucous membrane of the pylorus showed a typical cylindrical cell carcinoma, while the serosa of the same viscus revealed a pronounced colloid nodule as large as a walnut, which could not have arisen in any other way except by implantation from a colloid carcinoma of the cecum. Another mode of second- ary cancer formation is that of metastasis by way of the blood- vessels, these secondary neoplasms corresponding to the primary tumors in structure, and being recognizable, according to Grawitz, as secondary by their circumscribed character. These secondary forms are rare. The theory of infection for the origin of gastric cancers would not explain the great variety of the histogenesis of the carcinoma. In accepting the existence of a “ cancer-producing microbe,” one would have to assume that this organism could produce a trans- formation of connective tissue into epithelium, or that it regularly produced proliferation only in one kind of tissue — namely, the epi- thelial. A pathogenic micro-organism with these qualities is un- known at the present time. In the formation of metastases only the transported cancer cells keep on proliferating in the new organ, while the tissue of this organ either does not participate at all, or only to a small degree, in the formation of the new cancer nodule. THEORY OF INFECTIOUS ORIGIN OF CANCER. 543 In the transportation of tuberculous tissue, however, it is this tis- sue which breaks down, and the new tuberculous focus develops from the invasion of the transported tubercle bacilli, which not only cause a disease of the epithelium, but also of the remaining tissues (connective tissue, bone, etc.) with which they come in contact. Transplantation of carcinoma into animals has very rarely suc- ceeded, whereas inoculations of infectious diseases are generally successful. Another explanation of the development of cancer has been attempted in the so-called “ irritation theory,” which is based upon the susceptibility of the two openings of the stomach to greater irritation during digestion than other parts; these portions are consequently most frequently affected (sixty to seventy per cent, of all cases); but satisfactory proof that this irritation may cause cancer per se is wanting. We have elsewhere stated the percent- age of cancers occurring at various decades of life : According to the statistics of Welch, Brinton, and Lebert, three-fourths of all cancers occur from the fortieth to the seventieth year, and from the thirtieth to the seventieth year ninety-five per cent, of all gastric cancers manifest themselves. So far as we know, only one case of congenital cancer that was limited to the stomach has been reported (Wilkinson). There has been one case of congenital cancer com- bined with carcinoma of other organs (Widerhofer): We found in the literature on this subject a case of gastric cancer in a child five weeks old (Cullingworth). Three other cases in children some- what older are reported by Scheffer. (The subject of the etiology of cancer is reviewed in an interesting article by Roswell Park, “ N. Y. Med. Record,” vol. lii, No. i, July 3, 1897.) Heredity . — It is generally accepted that the predisposition to cancer may be inherited. According to Fleischer, the life insur- ance companies in Germany have increased their premiums for candidates in whose families gastric carcinoma has been observed. Napoleon I, his sister, and his father died of gastric carcinoma. Geographical Distribution . — The geographical distribution of gastric cancer is very irregular, for while it is very rare in some countries, — as in Turkey, Egypt, and the tropics, — it is said to be very frequent in Thuringen, in Suabia, in Normandy, and in Swit- zerland. The causes of this unequal distribution are unknown. In Egypt gastric cancers are unknown (Griesinger), but gastritis and enteritis are of common occurrence. This seems to show that a genetic relation between gastritis, enteritis, and carcinoma does not exist. According to Eichhorst and Haeberlin, two per cent. 544 MALIGNANT TUMORS OF THE STOMACH. of all deaths in Switzerland are caused by gastric cancer. From mortuary statistics, Tanchou (“ Rech. sur le Traitement Med. des Tumeurs du Sein,” Paris, 1844) estimates the frequency of gastric cancer as compared with that of all the causes of death at 0.6 per cent.;* Virchow, at 1.9 per cent.; Wyss, at 2 per cent.; and D’Espine, at 2)/ 2 per cent. In 8468 autopsies, chiefly from English hospitals, Brinton found gastric cancer recorded in 1 per cent, of the cases. Gussenbauer and von Winniwarter found gastric cancer recorded in 1 y 2 per cent, of the 61,287 autopsies in the Patholog- ical Anatomical Institute of the Vienna University. From an analysis of 11,175 autopsies in Prague, Welch found gastric cancer in 3 y 2 per cent, of the cases. Welch has collected and analyzed, with reference to this point, the statistics of death from all causes in the city of New York for the fifteen years from 1868 to 1882 inclusive, and reported that of 444,564 deaths during this period, cancer of the stomach was assigned as the cause in 1548 cases, and cancer of the liver in 867 cases. Some, at least, of these so-called cancers of the liver may be reckoned gastric cancers. This would make the ratio of gastric cancer to all causes of death about 0.4 per cent., and nearly 1 per cent. (0.93 per cenf.) if only the deaths from twenty years of age upward be taken, gastric cancer hardly ever occurring under that age. It is a fair presumption, also, that in New York not over 1 in 200 of the deaths occurring — at all ages and from all causes — is due to cancer of the stomach, and that about 1 in 100 of the deaths from twenty years of age upward is due to this cause. The following table (by William H. Welch, loc. cit .) gives the age in 2038 cases of gastric cancer, obtained from trustworthy sources and arranged according to decades : Age, . . . 10-20 20-30 30-40 40-50 50-60 60-70 70-80 80-90 90-100 Over 10 No. of Cases, 2 55 271 499 620 428 140 20 2 ■ Per cent., . 0. 1 2.7 13-3 24.5 3°-4 21 6.85 1 0. 1 0.05 From this analysis we may conclude that three-fourths of all * Tanchou’s statistics are based upon an analysis of 382,851 deaths in the Department of the Seine (see Welch, loc. cit ., p. 532). AGE AND LOCATION. 545 gastric cancers occur between forty and seventy years. The absolutely 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. Location. — The following table gives the situation of the tumor in 1300 cases of cancer of the stomach (from article by William H. Welch, loc . cit .) : Pyloric Region. Lesser Curva- ture. Cardia. Pos- terior Wall. Whole or Greater Part of Stomach. Mul- tiple Tumors. Greater Curva- ture. An- terior Wall. Fundus. 791 148 104 68 6 l 45 34 30 19 60.8 11 -4 8 5-2 4-7 3-5 2.6 2-3 i-5 per cent. per cent. per cent. per cent. per cent. per cent. per cent. per cent. per cent. From this table it appears that three-fifths of all gastric cancers 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 repre- sented by the cardia, the lesser curvature, and the pyloric region, is the part affected by gastric cancer. The lesser curvature and the anterior and posterior walls are involved more frequently than ap- pears from the table, inasmuch as many cancers assigned to the pyloric regions extend to these parts. The fundus is the least frequent seat of cancer. In the cases classified as involving the greater part of the stomach the fundus often escapes. Frequency. — Malignant disease is on the increase in this country . The death-rate from cancer in New York city was 1.82 per cent, from 1874 to 1884, but from 1884 to 1894 the death-rate from cancer was 2.17 per cent, of the total mortality (Jos. D. Bryant, the “Wesley M. Carpenter Lecture,” “ New York Med. Journal,” May 18, 1895). Haeberlin (“ Deutsches Archiv f. klin. Med.,” 1889, Heft, in und iv) gives the percentage of cancer of the stomach from 1877 to 1886 as 4.1 per cent. This writer has called attention to the fact 36 546 MALIGNANT TUMORS OF THE STOMACH. that in Switzerland also gastric cancer is on the increase; his figures, showing the death-rate from cancer of the stomach for 1000 inhabitants, are the following: 1877, 0.61 per cent.; 1878, 0.66 per-cent.; 1879, 0.72 per cent.; 1880, 0.77 percent.; 1881, 0.85 per cent.; 1882, 0.87 per cent.; 1883,0.85 per cent.; 1884, 0.84 per cent.; 1885, 0.90 per cent.; 1886, 0.99 per cent. In England the proportion of deaths from cancer to the total mortality rate was 1 in 129 in 1840. This had risen to I in 28 in 1880. The death-rate from cancer is now about four times as great in England as it was fifty years ago. The published figures of the Registrar- General’s report indicate that the mortality from cancer in the years from 1870 to 1890 has increased 53 per cent, in England. These facts are alarming and should stimulate the most diligent search for the cause of this disease. (For more complete statistics from various States and cities in this country see J. C. Hemmeter, “New York Med. Record,’’ Oct. 21, 1899, P- 577 *) (B) SARCOMATA. The sarcomata of the stomach are also classified into two groups according to their origin — namely, primary and secondary. The latter are by far the more rare. A single exception to this rule is the lymphosarcoma. The primary sarcoma of the gastric wall may develop from any place within the organ, but the greater curvature seems to be preferred, at least by such development as that in which tumor nodules (myosarcoma and fibrosarcoma) are formed, and in which no extensive lateral infiltrations are met with. There is a disposition on the part of some authors (H. Schle- singer, “ Zeitschrift f. klin. Med.,” Bd. xxxn, Supplement-Heft, S. 179) to separate the lymphosarcomata, on account of their different anatomical relations, from the other sarcomata. The point of issue of the latter group is either the muscularis or the submucosa, the mucosa not being diseased primarily. It may, however, become injured in the further progress by the arching forward of the tumor toward the interior of the stomach, resulting in lesions of the mucosa; in a purely mechanical way, from pulling and stretching; or it may become ulcerated toward the inner gastric cavity. In some cases the tumor may arch toward the peritoneal cavity. In the center of the sarcomatous nodules, particularly in the center of myosarcomata, processes of softening and disintegration, even of a purulent nature, may occur and give rise to septic peritonitis. These tumors possess a spherical or an irregularly knotty form, SARCOMA OF THE STOMACH. 547 and are attached by either a broad or narrow basis ; they some- times attain vast dimensions (Brodowski described a myosarcoma weighing twelve pounds). Metastases in neighboring organs, par- ticularly in the lymphatic glands, greatly modify the anatomical picture, duplicating, as to appearances, the original tumor. The tumors that have been observed so far are : Spindle-celled sarcoma (Hardy, Weissblum, Habershon, Tilger, Malvoz); angiosarcoma (Bruch); myosarcoma (Virchow, Kosinski, Kolisko, Brodowski); and fibrosarcoma (Tilger, Ewald, Dreyer). The majority of the round-celled sarcomata that have been described (Virchow, Cayley, Legg, Berry, Shaw, Drost, Rasch) are properly classed with the lymphosarcomata. W. Fleiner (“ Lehrbuch der Krankheiten der Verdauungsorgane,” Theil \,vide Magensarcom, S. 295 und 31 1) has clinically observed one case of lymphosarcoma and one case of round-celled sarcoma, and made histological studies of the same from the autopsies; and H. Schlesinger has given the clinical his- tory and undertaken the histological study of two cases of lym- phosarcoma and one of round-celled sarcoma of the stomach (Joe. cit.). The primary lymphosarcomata of the stomach seem to be rarer than the secondary form. In some cases the infiltration is limited mostly to the pyloric region, causing a rigid thickening of this part (Torok). In other cases it occurs in enormous infiltrations extending over the whole stomach, giving to the inner surface the appearance of a coarse swelling ; it may also have the appearance of a uniform infiltration. The mucous membrane may be pre- served for a long time in lymphosarcomata, but ulceration is not impossible. The spreading of the disease, as is usual with a lymphosarcoma, occurs by the lymphatic channels, those lymphatic glands that are nearest becoming diseased first, then the adjacent organs, and, lastly, the peritoneum. Sometimes no metastases occur, as in one case of Fleiner’s ; more frequently lymphosarco- mata are found as secondary neoplasms in the stomach after pri- mary tumors in other organs. In the cases of Kundrat (“ Ueber Lymphosarcomatose,” “Wien. klin. Wochenschr.,” 1893, No. 12) the original infected areas were the neck, pharynx, gums, and even the rectum. Symptomatology. — What is said here on symptomatology has reference to all neoplasms of the stomach. In a small number of cases the development of malignant growth of the stomach remains entirely latent, because every typical gastric symptom is wanting 548 MALIGNANT TUMORS OF THE STOMACH. until death.* As far as we have had occasion to observe, the first symptoms of a gastric carcinoma are those of chronic gastritis. Most of these patients state that, up to the time of their disease, they enjoyed a very good, sound stomach. The first dyspeptic complaints are those of pressure and fullness in the gastric region, eructations, anorexia, nausea, vomiting, cardialgia, and coated tongue. Disturbances of sensibility are not felt until the neoplasm has reached a certain size, thereby exerting pressure on the sensory nerves of the stomach ; or when, by its ulcerations, or by the irrita- tion of the digestive juices, these nerves have been exposed. The patient has a sensation as if a stone were lying in his stomach, some- times complaining of unpleasant feelings of emptiness, which come both at a varying time after eating as well as on an empty stomach, and not rarely continue an entire day, so that the patient is constantly reminded of his stomach, which he was not aware of formerly, and is placed in that characteristic despondent and mel- ancholic mood frequently met with in gastric sufferers. These sen- sations may increase to actual pain, which, however, is not so severe as in ulcer. Eructations are present in the beginning of gastric ulcer as well as later on, either bringing up air or small particles of the gastric contents, which have a bitter taste ; but, later on, when* in consequence of achylia, the stagnating gastric ingesta ferment more and more, the eructated gas may have a dis- gusting, decomposed odor and taste. Pyrosis may be present, and is, as a rule, accompanied by excess of organic acids. Singultus occasionally accompanies the eructa- tions, and is observed most frequently with carcinoma of thecardia. In rare cases (Ebstein and Eichhorst) there may be a tetany of the constrictor muscles of the pharynx, which is said to be caused reflexly from the stomach, and may prevent ingestion of food. The frequency of nausea and vomiting depends upon the location of the tumor in the stomach; they are never absent when the neoplasm is located at the cardia or pylorus. The nature and chemical condition of the vomited matter depend upon the time of the emesis and the degree of secretory disturbance as well as upon the extent of the gastritis, and may consist of more or less altered ingesta, decomposed food remnants, mucus, blood, or bile. Ad- *Friedenwald and Hotaling, “ N. Y. Med. Rec. Sept. 24, 1898, have collected the literature of a large number of such cases. Osier, “ Principles and Practice of Med.,” refers to several that were observed at the Johns Hopkins Hospital. PERISTALSIS, SECRETION, AND ABSORPTION IN CARCINOMA. 549 vanced decomposition is not observed until a late period of the growth. The vomited masses are rich in bacteria, and contain the Oppler-Boas bacilli, which are characteristic of lactic acid fermen- tation, though not pathognomonic of cancer (p. 129). The tongue nearly always has a brownish-yellow or grayish-white coating, but may be quite clean after profuse vomiting. The taste is said to be pasty, bitter, or offensive in the last stages, and salivation and thirst are increased. The loss of appetite belongs to the earliest symp- toms, with particular dislike for meat at all stages of the disease. In some patients complete anorexia alternates with bulimia. As a rule, appetite remains fair as long as there is any gastric secretion, or as long as the motility remains fairly good. Thirst is an annoying symptom in pyloric cancers, because they prevent the passage of water into the intestines — the stomach being incapable of absorbing water. Constipation and Diarrhea. — In the literature in which any refer- ence to these points was made, I found that in 75 per cent, of gas- tric cancers there is constipation, in 20 per cent, there is diarrhea, and only in 5 per cent, does the stool remain normal. The greater frequency of constipation is due to mechanical stenosis by tumor or to motor insufficiency due to carcinomatous invasion of the muscularis. Disturbances of Peristalsis , Secretion , and Absorption .« — These are caused by chronic gastritis, anemia, or direct extension of the neo- plasm into the mucosa and muscularis of the stomach. The dis- turbances of motility are either due to destruction of the muscularis or invasion of the gastric neoplasm, or to stenosis at the pylorus. We do not believe that they are traceable solely to the induced gas- tritis, because in chronic gastritis, according to very careful obser- vations, the motility in the majority of cases is not very seriously interfered with. Accordingly, we find that in from three to four hours after the test-breakfast, or eight to ten hours after a full test- dinner, when the stomach normally should be empty, an abundance of food remnants is contained in it. In cases where the neoplasm is not located at either orifice of the stomach, the motility remains good for a long time, and even in the absence of secretion of HC 1 , the vicarious digestion of the intestines is sufficient to make up for the loss of gastric digestion and to avoid emaciation. If it is desired to test motility in gastric carcinoma by means of our method, — that is, by the “ deglutable, india-rubber stomach- shaped bag,” — it is wise not to distend the bag too much ; in fact, 550 MALIGNANT TUMORS OF THE STOMACH. in cases of advanced cancer, the use of any intragastric instrument except the stomach-tube for this purpose is unjustifiable, because, in our experience, the stomach-tube, with the help of previous test-meals, has been found perfectly sufficient to ascertain the con- dition of the motility in this disease. The peristalsis may be studied in hospitals by means of the X-rays and capsules of bis- muth subnitrate swallowed by the patient (Boas and Levy Dorn, “ Deutsch. med. Wochenschr.,” 1898, 2). The course of the capsule can be readily observed by the fluoroscope. The loss of secretion in gastric cancer was first discovered by von der Velden (“ Deutsch. Arch. f. klin. Med.,” Bd. xxm, S. 369, 1879). The diagnostic value of the absence of free HC 1 in the gastric contents in malig- nant neoplasm is to-day universally admitted. There are other diseases (chronic gastritis and achylia gastrica) in which free HC 1 is absent, but it is one of the most constant symptoms of gastric cancer. Only in the carcinoma that arises from an ulcer do we find HC 1 present, and this is, in our opinion, explained by the fact that ulcus carcinomatosum is, in the great majority of cases, re- ported a very localized affection with little or no disseminating infiltration, and consequently does not destroy the glandular appa- ratus extensively. We should not conclude our study of the secre- tory function by merely testing for free HC 1 . In all cases an arti- ficial-digestion experiment should be made with egg-albumen discs, as described in the first part of this work, and the amount of the HC 1 deficit determined. I do not advocate this step as an accurate method of deter- mining the amount of combined HC 1 present; if information on this point is required, I recommend the methods of von Noor- denand Honigman, or the method of Martius and Luttke. Fortu- nately, the necessity for these analyses is very rare in practice. What is essential to know is how far behind the normal the HC 1 secretion is in suspected cancer cases, and for this purpose the determination of the HC 1 deficit is sufficient. The absence of free HC 1 in a large majority of cancer cases, when taken in conjunction with other signs and symptoms, has a high diagnostic significance. Although absence of free HC 1 occurs in chronic or atrophic gas- tritis and achylia gastrica, in progressed cardiac and pulmonary diseases and nervous anacidity these conditions are not easily mis- taken for carcinoma. Riegel formerly suggested that the HC 1 was destroyed by the carcinomatous tissue itself, or a product of it; later he inclined to the opinion, now generally accepted, that the STATE OF BLOOD AND URINE IN CARCINOMA. 551 loss of secretion is due to the accompanying gastritis or actual carcinomatous invasion of the secretory glands. As the stomach does not secrete HC 1 uniformly, — i. e., over all its surface, — it is conceivable that a carcinoma may occur in a portion where no HC1 is secreted normally, and in such a case HC 1 might continue un- disturbed as long as the neoplasm does not extend. The accom- panying gastritis may in other cases be limited, and therefore the glandular apparatus remain largely intact. We have observed six cases in which the presence of free HC 1 continued to the end of life. In two the neoplasm was seen during operation, and in the remaining four at autopsy. These six cases had not originated on the basis of an old gastric ulcer, but were rather circumscribed cancer masses in the pyloric antrum. Absence of accompanying gastritis, limited carcinomatous invasion of the acid-producing glandular portion, or location in the portion which normally secretes HC 1 , may serve to explain the cases of gastric cancers in which free HC 1 is still detected. They are so rare, however, that they can hardly invalidate the importance of the sign. Rosen- heim, Ewald, Hammerschlag, and the author have examined the mucosa from stomachs presenting carcinoma originating from ulcers ; previous test-meal analysis had revealed an amount of free HC 1 equal, on the average, to 0.12 per cent. No structural changes in the secretory glands were observed. The Jaworski method should not be neglected in testing for the prozymogens of the gastric ferments. About 200 c.c. of a 5 : 1000 solution of HC 1 are poured into the stomach, after it has been previously cleansed, and a quantity redrawn in twenty minutes; if this does not digest egg-albumen after a further addition of HC 1 , and no rennin-zymogen is contained in it, then the glandular activ- ity is completely extinguished. The state of the resorption is very much reduced, according to Eichhorst, Zweifel, Wolff, and others. Capsules of three to five grains of iodid of potash, which should give the iodin reaction in the saliva fifteen minutes after they are swallowed, do not, as a rule, give this reaction before one hour to one and a half hours have expired. With the progressive cachexia, the color of the face and of the external mucous membrane becomes pale or yellowish. There is persistent insomnia, and, as a consequence of the hydremia and the impoverished condition, the vessel walls become more per- meable, producing the frequent edema at the ankles and other dependent parts, which sometimes invokes suspicion of nephritis. 552 MALIGNANT TUMORS OF THE STOMACH. The body weight may be reduced thirty to forty pounds in from one to two months. The urine is greatly diminished in quantity, concentrated, and highly colored, as a result of the impaired absorption, frequent emesis, and edema. The reaction is neutral or even alkaline, particularly if, by methodical lavage, the acids and acid salts have been largely removed. An excess of indican is found in the urine. Von Jaksch demonstrated the presence of acetone in the urine, and Maixner discovered peptone in the urine of twelve cases he examined, and his results were confirmed by Parganowski. Maix- ner attributes the peptonuria to impairment of the ability of the gastric membrane to change peptone back into albumin, while Parganowski believes that the formation of the peptone takes place in the disintegrating cancerous tissue. The urine also gives a Burgundy-red color with chlorid of iron, which is probably due to diacetic acid. The feces frequently contain undigested muscle- fibers and egg-albumen taken in the food. There is pronounced constipation in seventy-five per cent, of cases, caused principally by stenosis of the pylorus, and in other cases by the greater amount of work that the intestine is called upon to perform and the im- paired peristalsis. In twenty per cent, of cases there is diarrhea, and regular evacuation in only five per cent. Special Symptoms. — Hematemesis . — The hemorrhages from gastric carcinoma are, as a rule, not abundant, although they are quite frequent. They are most frequently observed in carcinoma of the pylorus and of the lesser curvature. As hemorrhages which are not copious do not easily lead to emesis, there is suffi- cient time for changing of the blood pigments into hematin, which is uniformly mixed with the gastric contents, so that when they are eventually vomited, they present the appearance of coffee grounds or dark chocolate, which is, according to Brinton, a vomit that is observed in about forty-two per cent, of the cases, and is, therefore, an important sign in gastric cancer. This kind of vomit may also occur in chronic passive congestion of the stomach and in ulcer. In chronic gastritis one rarely meets with even small hemorrhage ; there is no diffuse staining of the ingesta, which simply shows streaks or points of blood. If the coffee-ground ad- mixture in vomit occurs frequently or daily for weeks, then it becomes an important pathognomonic symptom of gastric malig- nant neoplasm. The Occurrence and Determination of Tumor. — In all cases DIAGNOSIS OF GASTRIC TUMORS. 553 of suspected carcinoma of the stomach the examining physician should carefully and systematically go through the routine of in- spection, palpation, percussion of the entire abdomen, and artificial distention of the stomach by air or gas. When an abdominal tumor is formed by the dilated stomach itself, the diagnosis, in the majority of cases, can be made by a simple inspection. To deter- mine the presence of peristalsis in dilated stomachs, rarely anything else than close inspection is necessary. There are two conditions in which the stomach itself may form a palpable tumor by chronic contraction: one is where the organ shrinks in consequence of occlusion of the esophagus, and can be felt as a narrow, firm ridge lying below the left lobe of the liver; the other condition is known as cirrhosis ventriculi , and is the result of chronic hyperplasia of the walls, with subsequent contraction of the lumen. In very rare instances it may be caused by diffuse carcinomatous infiltration. The infiltrating scirrhous carcinoma of the stomach, even at the autopsy, may not be distinguishable microscopically from cirrhosis of the organ, the author having observed two such cases in which the nature of the gastric indura- tion was not discoverable from microscopical study of the sections from the stomach but only from the metastases. In this instance we are concerned most directly with the nodular and massive tumors of the stomach. As three-fifths of all tumors occupy the pyloric region, they should not escape diagnostic palpation, because in the majority of cases they displace the pylorus downward and render it palpable. When the stomach is filled with stagnating food or water, distended by gas, or in a state of atony, the pylorus is gen- erally below the edge of the liver. In some cases where the abdominal walls are not too thick, it is possible to feel and recog- nize the normal pylorus as a small, transversely placed ridge, which varies its position with respiration. Personally, I have occasionally been able to grasp the normal pylorus between the fingers of the left hand, and, by massage and compression of the fundus by the right hand, been able to recognize the escape of air and liquid ingesta through the pyloric ring. The detection of the location of the pylorus is easier in dyspeptic patients than in the normal state, because in cases in which it becomes important to recognize the pylorus there is generally considerable emaciation of the abdominal walls, thus facilitating palpation. Alternating relaxation and contraction of the pylorus may sometimes be felt, but this 554 MALIGNANT TUMORS OF THE STOMACH. phenomenon is very rare. Osier, in his “ Practical Monograph on the Diagnosis of Abdominal Tumors” (D. Appleton & Co., 1894), sums up the leading points concerning the solid tumors of the stomach in the following terms : “ Though only a small section of the stomach is available for palpation, a very large proportion of all tumors of the organ may be felt, owing in part to their greater frequency at the pyloric portion, and in part owing to the frequent depression of the organ.” He gives an account of twenty-four cases, in all of which a tumor or induration was detected. In the majority of the cases no trouble was experienced in determining whether or not a tumor was in the stomach. Excessive mobility of a pyloric growth and extensive infiltrating masses in the epigas- tric region were the only conditions causing trouble in any of the cases of his series. As other forms of tumor of the stomach (those that have I referred to in the sections on Malignant and Benign Tumors) are rare, a palpable tumor in the stomach may, as a rule, be considered a carcinoma. One can not exclude carcinoma even when a palpable tumor is absent, because twenty per cent, of all cases escape objective demonstration during their entire clinical history (Fleischer). Among these cases we must reckon the can- cers affecting the cardia, the lesser curvature, and part of those affecting the posterior wall. In order to instruct ourselves con- cerning the typical peculiarities of a tumor, and to avoid confound- ing it with neoplasms of adjacent organs, repeated and thorough examinations are necessary. The patient should be placed in a horizontal position, his knees should be flexed, and his mouth kept open, and palpation should be careful and gentle, because energetic and rapid palpation does more harm than good, as it produces an annoying tension of the abdominal muscles. We are in the habit of evacuating the stomach by lavage, and also the entire intestinal tract by a purge, prior to palpation, in order to bring about the most favorable conditions for this examination. Occasionally, a tumor will be evident upon simple inspection as a round or oval prominence, but the results of palpation are' more reliable. The cancer can be felt as a hard, uneven, sharply circum- scribed, nodular tumor. When the growth has extended more toward the interior of the stomach and brought about diffuse infil- trations, one feels a more uniform, and frequently only an indistinct, resistance toward the depths of the epigastrium or right hypochon- drium. In the beginning of a carcinomatous growth at the pylorus its smooth contour will not permit of a positive differentiation from POSITION AND MOVABILITY OF TUMORS. 555 benign hypertrophy, especially as the consecutive symptoms of stenosis, gastritis, and dilatation are coincident with both. In this case the only means of reaching a decision is by watching the further progress of the tumor. When the stomach is filled with food and gases, the tumor is less distinct on palpation. Per- sistent and stubborn reflex cramp of the pylorus may give the impression of carcinoma. In a case reported from Leube’s clinic, in a man aged ’thirty-six years, who had a dilatation and a distinctly palpable tumor in the umbilical region, an opera- tion was decided upon, but when von Heinecke and Leube reex- amined the man under chloroform anesthesia, the tumor had disappeared ; the patient was, consequently, not operated upon, and was reported living in good health twelve years after this experience. In two cases at my clinic gastric tumors were mimicked by sub- epidermic neoplasms of the skin. One was a negress with an elon- gate keloid tumor beneath the skin of the epigastrium, and the other was a white male who had been presented for operation for gastric cancer. On examination he was found to have a subcellu- lar lipoma in the abdominal walls over the epigastrium. Disten- tion of the stomach will prevent errors of diagnosis in such cases. Position and Movability of the Tumor. — Three-fourths to five-sixths of the normal stomach is located in the left half of the abdomen ; therefore one would expect that gastric tumors are generally palpable in the epigastrium a little to the left — rarely to the right — of the median line, and above the umbilicus. But as pyloric neoplasms are the most frequent (sixty per cent., Welch), these will be found to the right of the median line. Later on, the tumor sinks downward more and more and can be demonstrated below the umbilicus, particularly if it is a pyloric neoplasm. If no adhesions exist, it may even sink down into the pelvis. When there are adhesions near the locality of the tumor, it is immovable; but if they are absent, the tumor may be moved to-and-fro to some extent. Osier ( loc . cit.) gives some clear illus- trations of the positions into which gastric tumors can be moved. Changing the position of the body brings about a moderate move- ment in the growth. In order to ascertain whether a tumor belongs to the stomach proper, the changes in form and position of the organ, which are caused by filling the same with water or distending it with air, are very helpful. If on filling the stomach with water the tumor lies within the area of dullness thus artifi- 556 MALIGNANT TUMORS OF THE STOMACH. cially produced, and if on subsequent distention of the stomach with C 0 2 a tympanitic resonance can be made out above and below the tumor, it belongs to the stomach. On filling the colon with one to two liters of water the gastric tumors rise upward, and may hide behind the liver and sternum. It is generally stated that gastric tumors, in the majority of cases, do not move with respiration, but that tumors of the liver do. There are many exceptions to this rule. If there are any adhesions to the liver, spleen, or diaphragm, stomach neoplasms participate in the respiratory movements of these organs. If the tumor is of considerable size, it moves down- ward with respiration, because it can not get out of the way of the descending diaphragm. The percussion-note over the tumor is most frequently of a dull, tympanitic character. It has been stated that only hepatic tumors give a dullness on percussion, and that this may serve to differentiate them from the stomach tumors ; this, however, is a misleading sign, because large gastric tumors will give dullness on percussion, and if a hepatic tumor is located at the margin of the liver, or if a few loops of intestine or the colon lie between it and the abdominal wall, a tympanitic percussion- note will result. Pulsations may be evident in tumors that are adjacent to the celiac axis or superimposed upon the aorta. If the latter is compressed by the tumor, the tonicity of the crural pulse is diminished, and the epigastric growth may mimic an aneurysm. Differentiation of Gastric Tumors from Those of Adjoining Organs. — 1. From Splenic Tumors . — As gastric cancers rarely occur at the fundus, their differentiation from splenic tumors is rarely called for and is seldom difficult. The spleen is movable with respiration ; the stomach, only exceptionally. In splenic tumor we have dullness on percussion and absence of dyspeptic symptoms. In gastric tumor we have a tympanitic resonance on percussion and disturbances of secretion and motility. Splenic tumors can be very often mapped out and found to be ascending back of the ribs. 2. From Tumor of the Liver . — Hepatic tumors move with respira- tion, and frequently it is possible to grasp the gastric tumor and separate it from the liver. The contours of the liver should be determined, if possible ; for with hepatic tumors, the liver is gener- ally enlarged and sensitive to pressure, and the surface is frequently uneven. Phenomena of disturbance of hepatic circulation, such as icterus and ascites, denote liver tumor. It is true that dyspeptic symptoms may be secondarily caused by malignant disease of the DIFFERENTIATION OF ABDOMINAL TUMORS. 557 liver, but then they present themselves later in the disease ; with gastric cancer dyspeptic symptoms are among the very first.* 3. From Malignant and Other Tumors of the Gall-bladder. — Car- cinoma of the gall-bladder and accumulations of gall-stones may be confounded with pyloric carcinoma. The latter brings on gas- tric dilatation and grave anomalies of function, which are absent in affections of the gall-bladder. Cancers of the gall-bladder are not secondary to cancers of’ the stomach, as a rule. If, however, the gall-bladder tumor presses upon the pylorus, and also causes stenosis and dilatation, as we had occasion to observe at an autopsy in the Maryland General Hospital, the differentiation from gastric neoplasm is practically impossible. The assertion that hydrochloric acid is still secreted when the carcinoma is in the gall-bladder and not in the stomach, is not supported by sufficient evidence, because passive congestion of the stomach concomitant with gall-bladder and hepatic tumors often brings about loss of gas- tric secretion. 4. Carcinoma of the pancreas has frequently deceived clinicians in the diagnosis of abdominal tumors. Its immovability during respiration and palpation might suggest pyloric carcinoma; pan- creatic tumors, however, frequently cause stasis in the portal vein and pronounced icterus ; while dyspeptic disturbances and loss of HC 1 , which are early and prominent symptoms of gastric cancer, are absent. 5. Tumors of the Omentum and Peritoneum. — The differentiation of these tumors from gastric carcinoma is difficult when symptoms of disturbed gastric digestion are present and the tumor does not exceed the limits of the stomach. As a rule, these tumors, being secondary, are not so sharply circumscribed as are gastric tumors. Ascites is rarely absent. The original source — the primary tumor in some other organ — should, if possible, be discovered. Sometimes disease of the stomach may be excluded by chemical and micro- scopical methods, and then the diagnosis becomes possible. 6. Tumors of the colon , as a rule, sink downward, because the colon is very movable, unless (very rarely) adhesions form with the abdominal wall. By alternately filling the stomach with water and air, and subsequently evacuating it again, it may be demon- strated that the tumor is independent of the stomach. When the * The liver itself may give the signs and symptoms of a tumor (see chapter on Enter- optosis) . 558 MALIGNANT TUMORS OF THE STOMACH. colon is filled with one to two liters of water, the tumor rises but very slightly, if at all ; while tumors of the stomach, on filling the colon, generally ascend, and may disappear behind the liver or sternum. Tumors of the anterior wall of the colon become more distinct when it is filled with water, while those of the posterior wall become less distinct. A stenosis, as a rule, appears promptly, and the colon becomes tremendously expanded in front of the con- striction. Osier (loc. cil.) has reported a carcinoma of the cecum and colon, with enormous secondary enlargement of the liver, and extensive secondary nodules were scattered through the lungs. His case is very instructive, as the intestinal symptoms were ab- sent, thus illustrating the difficulty in making a correct diagnosis. 7 . Duodenal carcinoma can scarcely be separated from pyloric carcinoma. The occurrence of a tumor in the vicinity of the um- bilicus, the cachexia, the consecutive gastric dilatation, and (if the duodenal carcinoma should ulcerate) the coffee-ground vomit — all these signs may be present in cancers of either locality. If free HC1 can be demonstrated in the gastric contents, or its secretion can be caused after methodical lavage, the other symptoms of neo- plasm might possibly be referred to the duodenum. Carcinoma of the duodenum, as Ewald and Riegel have observed, may be com- bined with atrophic gastritis, so that absence of HC1 may, in these cases, occur, which absence is not directly caused by a gastric car- cinoma ; hence, the diagnosis is largely a matter of chance. The author’s method of duodenal intubation may be available in deter- mining a duodenal stenosis. It is evident that a thorough knowl- edge of gastric cancer and the application of all physical and chemical methods of diagnosis is necessary if we wish to be approximately correct in our diagnosis. In all cases of doubtful differential diagnosis exploratory laparotomy should not be de- ferred until the loss of strength of the patient contraindicates operation. Cachexia. — As the gastric cancer progresses, anemia and ema- ciation increase to a pronounced cachexia. The color of the skin becomes grayish-white or yellow; it may appear wrinkled, atrophic, and exfoliating. Frequently an annoying pruritus is present. The body weight becomes less and less the more digestion is disturbed ; the severer the vomiting, the more the passage of chyme into the intestine becomes obstructed. The blood grows more and more deficient in red blood-corpuscles and in hemoglobin, and a state similar to pernicious anemia may result. Pronounced diminution CARCINOMATOUS ULCKK. 559 of the hemoglobin is so constant an accompaniment of gastric cancer that it can almost be excluded in case the amount of hemo- globin is equal to sixty per cent, or more (Haberlin-Eichhorst). The amount may sink to forty and thirty per cent. In one case of Eichhorst’s it sank to ten per cent. Accidental sounds about the heart and signs of cerebral anemia or of moderate edema have been observed. Ascites is a consequence of secondary metastases in the liver or peritoneum, or of thrombosis in the portal vein; but toward the end of life it may be caused by great cardiac asthenia and hydremia. Thrombosis of the main vessels of one leg has been observed, and constitutes a very fatal sign. The pulse is mostly accelerated, and the body temperature is subnormal. Fever is a rare occurrence in gastric cancer; if it does occur, it is traceable to autointoxication with septic products formed in the ulceration or degeneration of the cancer. Coma carcinomatosum is a complication of symptoms similar to the coma of diabetics, and is accompanied by a peculiar, dyspnea. The respirations are strong and deep, and generally attended with a groaning sound in expiration. The rate of respiration is either normal or moderately increased. The temperature is either nor- mal or subnormal. There is no evidence of disease of the lungs or air-passages. It does not usually appear until anemia is far advanced. This kind of coma was first described by Petters and Kaulich, and later by von Jaksch (“Wien. med. Wochenschr.,” 1883, p. 473), and is probably a consequence of autointoxication. (See litera- ture of this subject in Albu, “ Autointoxicationen des Intestinal- tractus,” Berlin, 1895, p. 105.) As we have stated in the pathology of carcinoma, swellings of the peripheral lymph-glands are not rare at autopsies. A hard swelling of the supraclavicular glands was considered typical by Friedreich and Henoch. I find that, clinically, swelling of the cervical lymph-glands is a rare sign, and occurs only toward the end of the disease, by which time the diagnosis is generally clear. If severe vomiting ceases suddenly, a breaking down of the can- cerous infiltration of the pyloric region may be inferred, — by which communication with the intestines may be restored, — or it may be due to excessive muscular insufficiency. Carcinomatous Ulcer (Ulcus Carcinomatosum). — We have already stated, in the section on the Pathology of Gastric Ulcer, that atypical cell-proliferation may develop from a benign gastric ulcer, which thereafter entirely assumes the character of a carcinoma. 560 MALIGNANT TUMORS OF THE STOMACH. Rokitansky and Dittrich were the first to describe this condition, but Hauser (“ Das chronische Magengeschwiir,” Leipzig, 1883) gave the most accurate histological description of it. In 1891 Kollmann (“Berlin, klin. Wochenschr.,” 1891,5 und 6) reported fourteen cases, to which, up to the present time, as far as we know, about fourteen more can be added from literature. In this form of carcinoma the gastritis is, at the beginning at least, limited to the immediate neighborhood of the ulcer, or it may be entirely absent. Accordingly, the functional disturbances are less, and secretion may be normal, or we may even find hyperchylia. Very late in the course of this type the remainder of the mucosa may suffer from cancerous infiltration or gastritis, just as is the case with the ordinary gastric carcinoma, and then the functional disturbances become more pronounced. The diagnosis of carcinomatous ulcer can be made if a tumor can be recognized, together with normal or excessive secretion of HC 1 and a progressive cachexia. Of course, the previous history, which gives an account of years of gastric pain, — whereas cancer patients have, as a rule, when they present themselves not suffered so long, — is a valuable factor in the diag- nosis. If vomiting of blood or melena occurs in the clinical his- tory, the diagnosis becomes probable, but it is difficult to distin- guish between carcinomatous ulcer and the tumor-like induration of a large simple ulcer. It is also difficult to distinguish the carcinomatous ulcer from hypertrophic stenosis of the pylorus. Sometimes the recognition of secondary metastases in the liver, or other signs of cancerous dissemination, such as ascites and peri- toneal carcinosis, may be deciding factors. In one of our cases there was no tumor to be felt, only symptoms of cachexia and of gastric ulcer. For literature, see Rosenheim, “ Zur Kenntniss des mit Krebs complicirten runden Magengeschwurs,” “ Zeitschrift f. klin. Medicin,” Band xvn, Seite 1 16 ; also Boas ( loc . cit), second edi- tion, 1895, pages 188 and 189, and Hemmeter, “New York Med. Record,” volume lii, No. i i, September 1 1, 1897, page 365. D. D. Stewart has reported a case in which two isolated carcinomatous ulcers occurred in the stomach (“Am. Jour. Med. Sciences,” Nov., 1898). Perforations. — When a carcinoma perforates into other hollow organs, or exteriorly, life may be maintained for a short time, but perforation into the pleural or pericardial cavities, or into the lungs, rapidly leads to death. Gastrocolic fistulae cause very rapid emaciation, because the ingesta pass directly into the colon, in FRAGMKNTS SHOWING MITOSIS. 56 which very little digestion and resorption occur. With this kind of perforation, portions of excrement may be vomited. Bronchitis, traumatic pneumonia, and pericarditis may accompany the disease. Tuberculosis may be combined with gastric carcinoma. Diagnosis. — The majority of authors say that fragments of the cancer rarely occur in the vomit or are rarely brought up in the tube. In fact, it appears that the finding of carcinomatous parti- cles is considered an accident. It is probable that this occurrence is said to be so rare, not because these fragments do not occur in the vomit or wash-water, but because they are not methodically and systematically looked for. The great importance of an early diagnosis of carcinoma justifies the clinician in going to some trou- ble in order to find these fragments. We are in the habit of feed- ing all suspected cases for forty-eight hours by th^ rectum. Thereafter, the stomach is washed out with normal salt solution ; for this purpose we use a stomach-tube, which, though quite soft, is provided with an edge of the usual firmness around the lower opening. This tube, on being moved about in the stomach, is very likely to dislodge surface particles of the neoplasm. There is every reason why we should intentionally attempt to secure cancer particles from the stomach just as they are secured by cureting from the uterus. We have been able, in this manner, to find parti- cles of the neoplasm in the wash-water after it has been permitted to settle in a conical glass for about six hours, or after the solid particles were brought down with the centrifuge. When the sedi- ment in the bottom of the glass is first examined by a low power, and afterward by the higher power of the microscope, cells in a state of atypical mitosis can frequently be found. Previous to the rectal feeding, we wash out the stomach thoroughly in order to avoid confounding cancer particles with particles of meat, etc., retained with the ingesta. If this method is systematically followed, we believe that cancer particles will be more frequently found ; nor should we always deny the existence of carcinoma when we find no fragment giving the typical histological structure of these neoplasms, as described under their pathology. Whenever we find pieces of mucosa in which the glandular ducts are elongated and dilated, and the cells present numerous karyokinetic figures, and when asymmetrical and hypochromatic forms are found, the possibility of the existence of carcinoma should suggest itself, even when typical carcinoma cells are absent ; particularly when the interstitial tissue is considerably increased 37 562 MALIGNANT TUMORS OF THE STOMACH. and broadened, showing much small, round-cell infiltration when numerous eosinophilic cells are present and the parietal or oxyntic cells have disappeared, and are replaced by cylindrical or cuboidal epithelial cells, which proliferate down into the peptic ducts from the vestibular alveoli. Whenever cancer is suspected, the wash-water should be ob- tained from the fasting stomach in the morning, before any food is taken ; preferably, the contents should be drawn by the expression method without dilution, and any cellular detritus brought down by the centrifuge. In speaking of Rieder’s pioneer work in this direction, George Dock (“ Cancer of the Stomach in Early Life,” “Am. Jour, of the Med. Sciences,” June, 1897, p. 655) expresses himself as follows : “ It was therefore a matter of great interest when Rieder (‘ Deutsches Archiv fur klin. Med.,’ Bd. liv, H. 6, S. 544) reported a case in which he made a diagnosis of malignant disease of the peritoneum and pleura from finding numerous cells in the exudates, showing indirect nuclear division.” The patient was a woman of forty years. “ Section showed sarcoma (carci- noma?) of the peritoneum, probably secondary to malignant dis- ease of the ovaries.” In the fluids obtained during life, cells were found which were remarkable, “ in the first place, on account of the differences in size and shape of the individual cells. Often there were indentations and constrictions, sometimes buddings. In many cells there were one or many vacuoles, often so large that the nucleus was pushed to one side, sometimes hardly visible. The nuclei varied in size and number.” The examination of the stained cells showed large numbers of cells in a state of indirect division, and especially cells with atypical mitoses. “The most remarkable features of the sediment are presented by the great number of karyokinetic figures. These are especially common in cells from twelve to eighteen micromillimeters in diam- eter. The protoplasm of these cells is usually more homogeneous than that of others. Vacuoles sometimes occur, and in rare cases the protoplasm may be very much degenerated. Mitoses are so numerous that every field contains one or more. Often two to five can be seen in a small field. Various stages of nuclear and cell-divi- sion are present. The most common is that of the equatorial plate. The spirem and the monaster are uncommon. The metaphase is not so easily recognizable, partly on account of the obscurity of many of the figures. The anaphase is common.” Cells containing more than one nucleus, and with the nuclei in THE EARLY DIAGNOSIS OF GASTRIC CANCER. 563 different stages, are also common. In these cells one or more of the nuclei are in the resting stage, and one, or sometimes more, in vari- ous stages of indirect division and sometimes showing an atypical figure. The mitoses found, so far as they can be studied by the chro- matin alone, show all the common abnormalities. Thus, we find hypo- and hyperchromatic nuclei, the latter being rare. Giant mitosis may be represented by the tripolar figure. Asymmetrical mitosis is not easy to recognize, on account of the imperfect preser- vation of the chromosomes in many cases. The examples of mitosis in multinuclear cells resemble often the figures given by Krompecher (“ Ueber die Mitose mehrkerniger Zellen, und die Beziehung zwischen Mitose und Amitose,” “ Archiv f. path. Anat.,” Bd. cxlii, S. 447). The interesting history of atypical mitosis can only be touched on here. Eberth (“ Archiv f. path. Anat. und Physiol.,” Bd. lxvii) was the first to describe division into four parts, but his statements were at first discredited by Flemming and Strassburger. Later, however, Arnold (ibid., Bd. lxxxiii) found multiple karyokinesis in carcinoma. He thought the process might result in polynuclear cells. Since then a great deal of work has been done on this sub- ject, much of it being excited by the ingenious speculations of Hansemann. From an examination of the work done so far it appears that atypical mitoses are found in various pathological conditions, not only in new growths, like cancer and sarcoma, but also in benign tumors and in regenerations; in short, “in all tis- sues of strong reproductive activity and when there is active mitosis” (Strobe). They are also found in tissues irritated by various poisons, such as quinin, chloral, nicotin, etc., or in tissues exposed to high temperature (Galeotti). In cancer all observers find them in great richness and variety, but the view that the pres- ence of even a large number of pathological mitoses in a tissue justified the diagnosis of cancer is gradually being abandoned. As the literature is quoted in the works of Hansemann (“ Archiv f. path. Anat.,” Bd. cxix, S. 299, Bd. cxxm, S. 356, Bd. cxxix, S. 436 ; “ Studien fiber die Specificitat den Altruismus und die Anaplasis der Zellen,” Berlin, 1893), Strobe (“ Beitrage zur path. Anat.,” Bd. xi, xiv, Cornil (“ Journal de ’1 Anat. et de la Physiol. Norm, et Path.,” 1891, tome xxvn, p. 97), and Galeotti (“ Beitrage zur path. Anat.,” Bd. xiv, xx), it is not necessary to give a complete bib- liography here (George Dock, loc. citi). 564 MALIGNANT TUMORS OF THE STOMACH. Dock’s studies (Joe. cit .) concern only the exudates and transu- dates in suspected carcinoma of pleura and peritoneum. The author, in applying the method to examination of particles from carcinomatous stomachs, concludes that although the presence of a large number of cells in stomach-contents showing atypical mitosis is not pathognomonic of carcinoma, nevertheless it is very significant, and should stimulate further clinical investigation toward positive demonstration of existence of malignant gastric neoplasm. We have found in one case, four weeks before the tumor at the pylorus was palpable, portions of gastric mucosa, in which the glandular ducts were very closely packed, containing numerous leukocytes and showing a marked atypical appearance of the gland- ular epithelia, differing from the normal gland-cells by intense pig- mentation of the nuclei and much darker staining of the proto- plasm, together with marked increase of the connective tissue, small, round-cell infiltration, and in portions disappearance of the peptic cells, cylindrical epithelial cells having replaced them. In a second case an abundance of cells showing atypical mitosis were found after cureting the stomach, and the diagnosis of cancer made three months before a tumor became palpable, which at opera- tion proved to be a carcinoma of the posterior wall. There was no marked Uffelmann reaction for lactic acid in this case, but HC1 free and combined was absent at every test-meal. Such appear- ances in fragments should stimulate further careful and frequent examinations. Sooner or later, in our experience, a fragment will be obtained which will give the typical structure of carcinoma. Concerning the significance of the Oppler-Boas bacillus we have already spoken in the first part of this work. We can confirm the opinions of the authors quoted, that this organism is a very impor- tant diagnostic sign in this disease. My associate, Dr. Harry Adler, and myself have thus far examined fifty-five cases of gastric carcinoma, and found the organism present in fifty-two. Lactic acid is a valuable sign of intragastric fermentation, due to stagna- tion from dilatation and stenosis. It is not pathognomonic of gas- tric cancer, because it may not be present in excess even in cancer, provided the gastric peristalsis is unimpaired ; and, again, it may be present when the pyloric stenosis is due to a benign obstruction. However, as the majority of gastric cancers destroy the motility and cause obstruction, lactic acid, notwithstanding the exceptions reported (William S. Thayer), is a valuable diagnostic sign. See “A New Test for Lactic Acid in Gastric Contents,” J. P. Arnold, THE EARLY DIAGNOSIS OF GASTRIC CANCER. 565 “The Journal of the American Med. Association,” August 21, 1897. This is a modification of the chlorid of iron test, but not so accurate as that given on page 169. Lactic acid is formed in the stomach by the action of lactic acid bacilli on carbohydrates. Sticker has proved that the simple passage of carbohydrates through the mouth causes the formation of more or less lactic acid without exception ; the amount formed in this way is too small to be discovered by the Uffelmann test. Four conditions are necessary to effect excessive formation of lactic acid in the stomach ; these are: (1) Impaired gastric peris- talsis, which means stagnation ; (2) absence of, or great reduction of, HC 1 secretion ; (3) reduction of albumin digestion, and (4) im- paired absorption. Although there may be stagnation and reduc- tion or absence of HC 1 secretion, lactic acid will not form in the stomach if the proteid digestion is fairly good and does not fall below seventy-five per cent. Whenever there is much lactic acid in the stomach, the proteid digestion will usually be below fifty per cent, or entirely absent. The importance of impaired albumin digestion as a factor in the formation of lactic acid has been first emphasized by Hammerschlag and confirmed by Lindner and Kuttner. It is indispensable to investigate the combining power that proteids have for free lactic acid in this connection, for this organic acid can, to a certain extent, replace HC1 in proteolysis. If, as Hammerschlag points out, lactic acid is absent when albu- min digestion is perfect, or rather above seventy-five per cent., although the other conditions may exist, the question arises, How much of the already formed lactic acid may have entered into com- bination with the albumin of the food (in the absence of HC 1 ) and thus escaped detection ? (1) In the progress of gastric carcinoma the secretion of HC 1 suffers first (destruction of oxyntic cells) ; then (2) the formation of pepsin and rennin becomes impaired — the loss of pepsin brings on the defective albumin digestion ; (3) lactic acid fermentation fol- lows as a third step, requiring, in addition to the other two condi- tions, the factor of stagnation. The accuracy of the diagnosis, upon which the success of any possible operation must depend, is based on : (1) The recognition of tumors ; (2) the finding of cancerous particles in the wash- water; (3) demonstration of the Oppler-Boas bacillus; (4) the excess of lactic acid; (5) the absence of HC 1 and ferments, reduced or absent albumin digestion — by the filtrate of the gastric 566 MALIGNANT TUMORS OF THE STOMACH. contents; (6) the occurrence of hematemesis and melena ; (7) the loss of motility and presence of gastrectasia ; (8) the general symp- tomatology and anamnesis. The early diagnosis is possible only , as far as I can judge at present, by frequent microscopical examinations of curetings from the gastric mucosa which are very significant if they give evidence of numerous atypical mitoses. In any case, showing absence of HC 1 together with any one single sign of the others just enumerated, that does not improve under three weeks of treatment, exploratory laparotomy should be advised. (Hemmeter, “The Early Diag- nosis of Cancer of the Stomach,” “New York Medical Record,” October 21, 1899, p. 577.) Carcinoma of the Cardia. — Signs and Symptoms . — Complaints of an uncomfortable feeling, as of a foreign body, and of pressure above the gastric region, particularly after the ingestion of food. Sensations of pain are not contemporaneous with swallowing of food, but occur independently. On ingestion of food a sensation as if the same becomes clogged, or is caught before it reaches the stomach ; patients imagine that copious drafts of water give 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 retching up of mucus and a few food particles containing no HC 1 . The cause of these regurgita- tions of masses of mucus is the formation of a large dilatation of the esophagus above the stenotic carcinoma of the cardia. In this esophageal diverticulum or dilatation the food is caught, retained, putrefies, and is eventually vomited up again. There is also a septic catarrhal esophagitis present at this place. Liquid or semi- liquid substances may for a long time be able to pass, while rela- tively 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 uninterruptedly. If an obstacle to the passage of the sound can be ascertained at the entrance to the stomach in a person over thirty years of age, the diagnosis of cancer of the cardia becomes certain. In all such suspected cases only a soft elastic tube should be used for explora- tive sounding. In a number of cases in private practice I was enabled to establish the diagnosis by microscopical examination of small portions of the carcinoma that were brought up with the sound. These neoplastic fragments are occasionally found in the eye of a lower opening of the sound, and they constitute a definite DIAGNOSIS OF CARCINOMA OF THE CARDIA. 567 criterion. In one of the foregoing cases the diagnosis was con- firmed by Dr. M. Einhorn, and in the other by autopsy. In addition to the sounding and the cancerous fragments, the follow- ing signs are of diagnostic importance : 1. Percussion of the region over xiphoid cartilage is very painful. 2. On the sound blood will frequently be found mixed with the extremely fetid 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. 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, sup- ports the diagnosis, but this is a rare sign in my experience. 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. Duration of the disease is six to nine months after the first symptoms are manifested ; death occurs as a result of gradual exhaustion, marasmus, aspiration pneumonia, secondary carcino- mata in the liver and other organs, and intercurrent hemorrhages. Differential diagnosis from chronic gastritis is difficult in the beginning of cancer of the cardia, 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 eso- phageal 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 frequent), by the hematemesis and the bloody stools of ulcer. Ulcer of the esophagus 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 esophagus. The permeability of the gullet will be more variable than in cancer, because the sound will often skip the diverticulum. In the latter there will rarely be pain, and the marasmus will not be so progressive and rapid. From cardiospasm, or cramp of the cardia, the carcinoma is differentiated by the occasional free passage of the thickest tubes in the neurosis, 568 MALIGNANT TUMORS OF THE STOMACH. which occurs almost exclusively 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. Syphilis may be excluded or diagnosed by the effect or non- effect of specific treatment, and tuberculosis by the effect of hypo- dermic injection of minute doses of tuberculin. Treatment of Cardia Carcinoma . — So long as there is no cure possible, this must be palliative. During the time that deglutition still brings liquid food into the stomach, the sufferer must be care- fully fed on highly nutritious liquid diet — liquid eggs and wine, as described in the diet of gastritis, beef-tea, soups of fluid potato or pea puree in bouillon, Leube-Rosenthal beef-solution, von Mehr- ing’s “ Kraft ” chocolate, egg'-nog. When pain was great, I have found that chloral hydrate (15 grains, three times daily) not only relieved it, but acted as a local disinfectant in the diverticulum above the stenosis. Boas recommends iodid of potassium in doses of 15 grams, three times daily, as aiding in keeping the esophagus from closing up as soon as it would otherwise. Arsenic is said to effect the same prolonged permeability. I have had no success with these drugs in my cases. In one case I succeeded in keep- ing the esophagus open for six months by intubating with an in- elastic tube four inches long and as wide as an ordinary Ewald tube. The tube was removed every ten days and replaced. Patient lost no weight in those six months, but even gained. Death was caused by aspiration pneumonia, during a period in which the tube was left out in order to wrest the esophagus from the stout cord by which the tube was connected with the mouth, and which was usually tied around the 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 and the. shock of the operation is better borne. This operation consists in making an opening into the stomach for the purpose 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 from the immediate results of the operation. Zesas (“ Archiv f. klin. Chirurg.,” Bd. xxxii, S. 188) reported 13 1 cases from literature, mostly esophageal cancers, which in their stenosing effects are identical with those of SIGNS IN CARCINOMA OF THE BODY OF STOMACH. 569 the cardia. Among these only 19.5 percent, recovered sufficiently from the operation to call this a success. Carcinoma of the Body of the Stomach and of the Pylorus. — ( Cancer of the Fundus , Anterior or Posterior Walls , the Curva- tures , and Pylorus .) Subjective Signs. — 1. Sudden abrupt beginning of the disease, striking an apparently healthy organ. 2. Loss of appetite in 90 per cent, 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. 7. There is frequent vomiting, which is more copious in pyloric cancers because of the accumulations from the dilatation. Frequently the vomit has a coffee-ground appearance, and the hemin test (referred to in part 1) proves the presence of blood. The state of the bowels is variable, but constipation occurs in 75 per cent. The vomit contains, as a rule, no hydrochloric acid, but excess of lactic acid and Oppler-Boas bacilli. Objective Signs. — On inspection, palpation, and percussion a tumor can be made out in at least 50 per cent, of the cases. Tumors of the pylorus do not move with the respiratory move- ments unless attached to the liver ; tumors of the curvatures gen- erally show distinct respiratory movements. Examination of Stomach- Contents. — The results will be character- istic in most cases, and evince — 1. Grave interference with the motility. 2. Suppression of secretion. 3. Reduced or absent albumin digestion. 4. Products of stagnation dependent upon these. 5. Fragments of neoplasm or mucosa showing characteristics previously described. The disturbances 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 lavage 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 hydrochloric acid and presence of lactic acid, are found in 88 percent, of the cases in our experience. In carcinomata that 570 MALIGNANT TUMORS OF THE STOMACH. have arisen from old ulcers, a secretion of hydrochloric acid per- sists until the last stages of the disease. This assertion of Rosen- heim’s is not always correct; if the glandular layer is invaded, secretion must cease, no matter whether the carcinoma arose from an ulcer or not. The fact that carcinomatous ulcers do not destroy the secretion of HC 1 , as a rule is due to their anatomical location — they occurring mostly in the pyloric region, which does not contain the oxyntic cells in abundance. Lactic acid is tested for by Uffelmann’s reaction ; in carcinoma there is an excess in from 78 to 90 percent, of the cases. Demonstration of the long, base-ball- bat-shaped Oppler-Boas bacillus is, according to Kaufman, Schle- singer, and Riegel, a very important sign. There should always be a careful lookout for histological evidences, such as bits of the growth in the wash-water and vomit ; this clinches the diagnosis. Secondary symptoms are anemia, cachexia, and edema of the ankles in 15 to 20 per cent, of the cases. The urine contains excess of nitrogen excretion, indican, and peptone. Latent cancers may occur ; they are very rarely observed, however, at the autopsy. Ulcus Carcinomatosum . — The diagnosis is made from a history of ulcer, with years of gastric pain, — not a sudden and abrupt begin- ning, — and the presence of hydrochloric acid, even hyperacidity. A previous history of hematemesis and blood in the stools points to origin of the carcinoma from ulcer. Simple, uncomplicated ulcer may cause a tumor-like thickening, simulating cancer ; here the analysis of gastric contents may, in rare cases, even show excess of lactic acid, owing to motor insufficiency and cicatricial stenosis, and the diagnosis then becomes difficult, as is also the differential diag- nosis of ulcus carcinomatosum from simple hypertrophic stenosis of the pylorus. Fortunately, such states without any other impor- tant signs are rare. Treatment . — There is no successful medicinal treatment for this disease. Life may be prolonged by a suitable diet, as nutritious as possible and adapted to the individual conditions. A highly nutri- tious proteid, carbohydrate, and fatty diet should not be interdicted so long as the motility is good and the patient’s strength can be upheld by intestinal digestion. When there is stagnation owing to pyloric obstruction, the carbohydrates and fats must be diminished. The best tonic for the stomach is daily lavage, even when there is not much stagnation ; but when the latter is marked and accom- panied by fermentation, antiseptics may advantageously be added — such as boric acid, 20 to 30: 1000 H 2 0 ; salicylic acid, 3 : 1000 TREATMENT OF GASTRIC CANCER. 571 H 2 0 ; sodium benzoate, 10 to 30: 1000 H 2 0 ; resorcin, 10 to 30: 1000 H 2 0 ; thymol, 5 : 1000 H 2 0 ; lysol, I to 2 : 1000 H 2 0 ; hydrochloric acid, 4 to 5 : 1000 H 2 0 . It is always well to get the stomach clean by simply using warm salt solution, and to finish the lavage by a last irrigation with one of the disinfectants, of which we pre- fer hydrochloric acid. A tonic which has been serviceable in my experience and which will arouse appetite and promote digestion in the invaded organ, if this is at all possible, is the following : K • Extract, condurango, 45 ° c.c. f^xij Strychnin, sulph., 0.021 c.c. gr. Acid, hydrochloric, dil. , 12.0 c.c. f^iij Elixir gentianse, q. s. 180.0 c.c. f;|vj. M. SlG. — Take one tablespoonful in two ounces of water, after meals, through a tube. When there is much anemia, the following formulae has my preference in this disease as well as in ulcer : 1 £ . Solution of iron and manganese, . . . 186.60 grams Liquor potassi arsenit., 3.0 grams SlG. — One tablespoonful three times daily. Or — H. Strychnin, sulph., 0.02 grams Elix. gentian, cum ferri chloridi, . q. s. 186.60 grams SlG. — One tablespoonful three times daily. Constipation is best met by large colon irrigations or with the fluid extract or active syrup of cascara sagrada (Clinton). Diarrhea must be met by salol, bismuth salicylate, or benzo- naphthol. Opiates are not advisable for this symptom unless there is pain. For pain hot external cataplasms and 20 to 30 drops of com- pound spirit of ether should be first tried. If severe, codein (gr. extract, belladonnse (gr. in f§j of peppermint water, gener- ally relieves it, and may be repeated if requisite. The pain is rarely so intense as to require hypodermic injections of morphin. Lavage systematically and scientifically employed seems to prevent pain ; it certainly prolongs life, and sometimes apparently works wonders for these patients. For the diet in gastric carcinoma we refer to the chapter on Dietetics, pages 203 and 240. Fifty grams of rich milk or a glass of tokay, a few crackers, and chocolate are permissible foods; also young pigeon, partridge, and f .l v j rr^xlviij. M. g r - l A Svj- M. 5;2 MALIGNANT TUMORS OF THE STOMACH. prairie-hen. If the motility is good, one must not be too severe on the patient’s desire for food ; many cases can live and gain strength on an ordinary nourishing diet when it is not retained too long in the stomach ; under these circumstances mutton chops and broiled beefsteak, finely minced, may be allowed. Surgical Treatment. — As already mentioned, gastrostomy is a palliative operation for malignant tumor of the cardia and esopha- gus, to permit of direct introduction of food by establishing an opening between the stomach and the abdominal wall. In carcinoma of the pylorus another palliative operation is practised — when it is impossible or inexpedient to remove the growth — under the name of gastro-enterostomy. This consists in the establishment of a new communication between the stomach and the small intestine, thus allowing the chyme to reach the intestines without passing the pylorus. The radical operations are resections of the pylorus or excision of the tumor, no matter where it may be situated in the stomach. These operations are contraindicated if metastases are detectable in other organs, by the presence of great anemia or cachexia, by the large size of the tumor, or if there are adhesions to other organs. The detailed descriptions of these operations belong to text-books on abdominal surgery : See “ Surgery of the Alimentary Canal,” by A. Ernest Maylard ; P. Blakis- ton’s Son & Co., Philadelphia, 1896. “The Cartwright Lectures on Gastric Surgery,” by W. W. K'een, “ Phila. Med. Jour.,” volume 1, 1898. “ Abdominal Surgery,” by J. Grieg Smith, published by P. Blakiston’s Son & Co., Philadelphia, 1896. “ Surgery by American Authors,” by Roswell Park, volume 11, chapter viii, published by Lea Brothers, Philadelphia. “System of Surgery,” by Fred. S. Dennis, volume IV, page 217. “ Abdominal Surgery,” by M. H. Richardson and Farrar Cobb. “ A Text-book of Abdominal Surgery,” by Skene Keith and G. S. Keith. Frederick Treve’s “ Manual of Operative Surgery,” volume 11, page 405. Franz Koenig, “ Lehrbuch d. speciel. Chirurg.,” Band 11, Seite 281. Penzoldt and Stintzing’s “ Handbuch d. speciel. Therapie,” volume iv, page 444. (“ The Operative Treatment of Gastric Disorders,” by Professor von Heinecke, Erlangen.) The Course to Pursue in Practice. — Occurrence and Detection. — With the exception of the cases that arise from ulcer, cancer of the stomach, as a rule, develops gradually. Among the phenomena are symptoms of more or less severe dyspepsia, gradually ranging THE COURSE TO PURSUE IN PRACTICE. 573 to the most decided ones of chronic gastritis, which, almost with- out exception, accompany every carcinoma of the stomach. Therein lies a great hindrance to timely detection. If, however, — and this especially in older individuals, — the symptoms of chronic gastritis appear without any distinct cause, and in a stomach previously entirely sound, and get worse constantly, even with a mild diet, and are increased by pains and vomiting even before food is taken (with a jejune stomach), so that in a few weeks rapid emaciation, with an extraordinary sallow complexion, become pronounced features, carcinoma of the stomach should be suspected. What are the characteristic and most important diagnostic signs of gastric carcinoma? Examination with the stomach-tube is to be made, and the reaction for free acid in the contents of the stomach which have been brought up one hour after the test- breakfast is to be tried. In any case the treatment with lavage is to be instituted, and with it the most frequent repetition of the test for free acid. In this connection it is well to make examination of the juices after several test-meals, and eventually with means stim- ulating the secretion of acids (orexin) ; but, of course, always at a time when, under normal circumstances, free acid ought to be present. Protracted absence of free hydrochloric acid, even though it may occur in other diseases of the stomach, speaks, in the method of procedure indicated, with great probability for cancer, since in more than ninety per cent, of the cases HC1 was found absent. Frequent presence of hydrochloric acid argues against cancer. Repeated examination with the tube brings us other signs of carcinoma, which by other observations are not — or, at any rate, not so easily — obtained. Occasionally a particle of the cancer is found in the vomited masses, and the diagnosis is made sure. This may happen more easily with lavage in the wash-water from carcinoma of the cardia, when it may also be found in the eye of the tube. During methodical lavage, coffee-ground vomit is seen earlier and more frequently than if we depend upon the vomiting. In the latter case it is often poured away before the physician gets a chance to examine it. In case of carcinoma one does not need to fear hemorrhage in using the tube, provided it is done carefully. Finally, one may also use the contents of the stomach obtained with the tube for the quantitative and qualita- tive determination of the lactic acid. An approximately simple method for this purpose has been recently published by H. Strauss, of Riegel’s Klinik (“ Berlin, klin. 574 MALIGNANT TUMORS OF THE STOMACH. Wochenschr.,” 1895, No. 37). Excess of lactic acid has been found in eighty-two per cent, of my cases. It is true that it has also been shown to exist with gastritis and hypertrophic benign stenosis of the pylorus, which somewhat diminishes its value. It is not an early sign in this disease. But still, as it appears at present, in connection with other signs it is valuable for the diagnosis, even though its absence does not argue against carci- noma and was especially observed in carcinomatous ulcer. It will therefore be possible in many cases to fix the diagnosis with a great degree of probability, even before a tumor is palpable, when elderly persons previously sound grow rapidly worse in spite of suitable treatment, and when cachectic symptoms ap- pear quickly, when the absence of free hydrochloric acid con- tinues, or when there is vomiting of coffee-ground masses. Since, ordinarily, the tumor can only be felt when the cancer has reached a certain size and lies in an especially favorable posi- tion, the diagnosis by recognition of a tumor is generally no longer an early diagnosis. The examination in chloroform narcosis must be brought in at a comparatively early date to facilitate pal- pation, and with a sufficient degree of insensibility it will indeed very much facilitate the detection. Distention with air through the stomach-tube renders a tumor at the front wall or at the pylorus more distinctly recognizable, and gives information con- cerning the size of the stomach. Distention of the intestine in narcosis by means of air is also brought in as an aid to the diag- nosis. If it is not possible to feel a tumor, and if, in spite of this, one is convinced that a neoplasm does exist, one should propose an exploratory incision, with eventual further operative procedures if the prospects warrant immediate good results. If carcinoma should follow apparently in the course of gastritis or ulcer, the diagnosis becomes more difficult than if it is developed in an apparently healthy stomach, for then the symptomatology, the state of the secretions, and the proof of the presence of lactic acid or hemor- rhage are of much less value. Then the diagnosis requires the greatest circumspection. Since the detailed description of all the possibilities does not suit the compass of the work, we will here only refer again to the fact that, with rapidly increasing emacia- tion of the patients, the physician must not rest until he has found the causes in a carcinoma, or in another factor, such as stenosis of the pylorus. In all chronic cases with the chemical and physical signs described, exploratory laparotomy is urged if improvement does not follow in three weeks of appropriate treat- TREATMENT OF INDIVIDUAL SYMPTOMS. 575 ment. In cases in which the carcinoma causes no symptoms, or only very indefinite ones as regards the stomach (for instance, in the case of people advanced in age), the diagnosis is, of course, impossible, and active treatment not so important. If there is a pal- pable tumor in the region of the stomach, we have the problem of determining that the same is really a new formation belonging to the stomach. From the therapeutic standpoint, one is to avoid con- founding it with tumors which either need not be or can not be operated. Among the former are to be mentioned the normal head of the pancreas, which with severe emaciation might be mis- taken for a carcinoma; lymphatic glands, which are felt as small smooth nodules alongside of the spinal column, and may be quite harmless (Leube); tumor of the spleen, which can not be grasped from above; movable kidney, which is smooth, and which gives the kidney shape. Of the nonoperable tumors, or only exception- ally operable, we should exclude cancer of the liver, which, with- out the characteristic gastric symptoms of the stomach, causes the liver to appear enlarged and much distended, or causes nodules to appear on the palpable lower edge (see the extension of the cancer from the stomach to the liver). Gall-bladder and omental carci- nomata are chiefly to be excluded from diagnosis by the absence of the conspicuous stomach symptoms, and the latter by the want of respiratory movability and by the presence, generally, of ascites. Carcinoma of the mesenteric glands is, under some circumstances, not to be distinguished from that of the stomach. Penzoldt recently observed a case which had, in addition, violent hemat- emesis and stomach symptoms. The differential diagnostic points from tumors of the duodenum, colon, and neighboring organs have already been considered (pp. 556 to 558). DIET FOR GASTRIC CARCINOMA. — {Rosenheim.) 8 a. m. — One cup of tea with milk or a farinaceous soup, eventually with a little wheat bread. 10 A. m. — Toast, sardels, caviar, perhaps also oysters, with good claret, sherry, or Madeira. 1 P. m. — Bouillon or soup (flour, rice, sugar, and tapioca soups), eventually with addition of peptone, or Leube-Rosenthal’s meat-solution. White meat or game, or beefsteak from finely scraped beef, or jellies with gravy, or calves-feet. Vegetables. Potato puree, finely chopped spinach, well cooked asparagus. Stews : Stewed apples, pears, prunes (without hulls). Drinks : Red wine, water with cognac. 4 p. m. — Meat peptone, chocolate or cocoa with cakes. 7 p. m. — Bouillon and soup from leguminous flour. 576 MALIGNANT TUMORS OF THE STOMACH. For further diet for gastric carcinoma see chapter on Dietetics. Treatment of Loss of Appetite. — Of the so-called stomachic remedies, condurango is useful in this disease. We prefer the officinal fluid extract of condurango. The other stomachics and bitter tonics used are the tinctures of calumbo, gentian, cinchona, etc. ; likewise hydrochloric acid, which, however, does not always agree with the patient. Orexin generally has no effect, but an attempt with 0.2 to 0.3 gm. of orexin basicum should be made. Also, lavages of the stomach with decoctions of hops and quassia wood, according to Kussmaul and Fleiner, may be used with ad- vantage. Washing the stomach remains the best means for excit- ing the appetite. Treatment of Vomiting. — Against vomiting we recommend : Small quantities of ice, ice-cold water containing carbonic acid or champagne, a few drops of chloroform, tincture of iodin, creasote, morphin subcutaneously or as a suppository, cold bandages on the epigastrium. If it is a consequence of stagnation of foods in the stomach, lavage is the most efficacious treatment. If the vomited matter has a foul smell, and foul belching is present, one may add thymol (0.5 per cent.), boric acid (two to three per cent.), salicylic acid, resorcin, chloroform (0.5 per cent.), to the wash-water. The treatment of hemorrhages is the same as for gastric ulcer. Treatment of the Pain. — Steam vapor, bandages, and poultices, hot cloths, or plates have only a temporary success. If the pains are very violent, one can not avoid the subcutaneous injection of morphin, but care must be exercised to avoid starting the morphin habit. Treatment of Constipation. — This very frequent and troublesome symptom must be eliminated, if possible, by large colon irrigations (one liter), by injections of water with the addition of soap, turpen- tine, castor oil, etc., which increase their effect, or by the injection of glycerin. Only when this is of no avail must recourse be had to the vegetable purgatives — e. g., Extr. aloe, Extr. rhei comp., aa 3.0; addeSucc. liq., q. s. ft. pil. 30. M. One or two pills at bedtime. Saline purgatives are justly objected to, since they weaken the patient to a remarkable degree. For the same reason Penzoldt, Ewald, and Lebert declare that drinking cures at Carlsbad and other saline springs are not advisable. This prohibition is gen- erally very hard for those patients who have placed all their hope on a sojourn at the springs. The advice of Lebert (quoted by Ewald), to let them drink small quantities of the mineral water LITERATURE ON CANCER OF THE STOMACH. 5 77 at home, is very practical, for generally it is without success, and the patient will then willingly give up a trip to the springs. If the constipation is due to stenosis of the pylorus, medicines by the mouth are useless. So the treatment, briefly, is lavage, tonics, rest, the most highly concentrated and nutritious food, whenever it is too late or impossible to operate. Prognosis. — If the diagnosis can be made early, and operative treatment gives fair prospects of immediate good results, there is, as we have seen from the statistics given in the chapter on Surgical Operations (p. 348), some hope of prolonging life. But if an opera- tive interference is impossible (see the contraindications, p. 366) or refused, the disease must prove fatal. Careful dietetic and mechanical treatment may, in individual cases, prolong life for several months. In cancerous neoplasms that do not affect the orifices the immediate danger is not so great. I have reported a case in which a positive diagnosis of malignant tumor could be made from a cancer particle that came up in the wash-water and in which a tumor was diagnosed by Da Costa and Musser sixteen months before the author examined the patient. This patient lived two years and two months after the tumor was first recognized. LITERATURE ON CANCER OF THE STOMACH. 1. Aaron, C. A., “ The Early Diagnosis of Cancer of the Stomach,” “ Canada Lancet,” i 897-’98, xxx, 395-398. 2. Acker," Zur Pathogenese der Geschwulstmetastasen,” “ Deutsche Archiv f. klin. Med.,” xi. 3. Aisberg, " Casuistik zur Chirurgie der Magencarcinoms ” ; "Drei Falle von Gastro-enterostomie, im dritten Verlangerung des Lebens um drei Jahre und fiinf Monate,” " Miinch. med. Wochenschr.,” No. 50 und 51, 1896. 4. Arnold, J., “ Ueber Theilungsvorgange in den Wanderzellen : ihre pro- gressive und regressive Metamorphose,” "Archiv f. mikr. Anatomie,” XXX, 1887. 5. Arnold, J. P., “ Colloid Cancer of the Stomach,” " Proc. Path. Soc.,” Phila., 1897-98, 1, 305. 6. Badaloni, N., "Del cancero dello stomaco,” " Gazz. de. osp. Milano,” 1897, xviii, 705-740. 7. Bazy, " Cancer de l’estomac, gastro-enterostomie ; avec le bouton de Murphy,” " Bull, de la Soc. de chirg.,” xix, 1896. 8. Benedict, A. L., "Some so-called Diagnostic Points of Gastric Carci- noma,” “ Int. Med. Magazine,” Phila., i 897~’98, vi. 9. 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Strube, Geo., “Trichomonas hominis in the Gastric Contents in Carci- noma of the Cardia,” “Berl. klin. Wochenschr.,” Aug. 8, 1898. 193. Strube, Geo., “ A Case of Cancer of the Pylorus Presenting Some Unusual Features,” “Lancet,” Oct. 1, 1898, vol. 11. 194. Stucky, T. H., “Malignant Disease of the Pylorus,” “ Internat. Clin.,” Phila., 1898, 8, 3. s. 159-163. 195. Szekacs, B., “ Ein Fall von Magenkrebs mit intermittierendes Fieber,” Budapest, koz korhazak eokonyve, 1894, rol Budapest, 1896. 196. Thayer, W. S., “Johns Hopkins Hosp. Bullet.,” 1893, No. 31. 197. Thoma, “Ueber eigenartige parasitare Mikroorganismen in den Epi- thelzellen der Carcinome,” “ Fortschritte der Medicin,” 1889, No. 2. 198. Tuffier et Dujarier, “ Perigastrite gangreneuse anterieure suite de can- cer gastrique,” Soc. Anat. de Paris*, 14. Janv., 1898. 199. Uffelmann, “ Ueber die Methode der Untersuchung des Mageninhalts auf freie Salzsaure,” “ Deutsches Archiv f. klin. Med.,” 1880, Bd. xvi. 200. Ullman, J., “ Gastric Carcinoma ; the Presence of the ‘ Faden ’ (Oppler- Boas) Bacillus as an Important Factor in Gastric Carcinoma,” “ Buffalo Med. Jour.,” i898-’99, N. S., xxxviii, 18-23. 586 MALIGNANT TUMORS OF THE STOMACH. 201. Vedel, “ Cancer de l’estomac avec perforation et abouchement dans une masse ganglionnaise peritonite aigue fibrineuse,” “ Nouv. Montpellier med.," 28 mai, 1898. 202. Von den Velden, “ Ueber Vorkommen und Mangel der freien Salzsaure im Magensafte bei Gastrectasie,” “ Deutsch. Archiv f. klin. Med.,” 1879, Bel. XXIII. 203. Verstraete, “Deux cas de cancer de l’estomac,” “J. d. sc. med. de Lille,” 1898, 1. 204. Vickery, H. F., “A Report of Three Cases of Cancer of the Stomach in which Hydrochloric Acid was Present,” “ Boston Med. and Surg. Jour.,” 1897, cxxxvii, 132. 205. Vilcog et Lancy, “ Cancer de l’estomac, pyemie streptococcique second- aire,” Soc. Anat. de Paris, 19, vi, 1897. 206. Virchow, “ Bemerkungen fiber die Carcinomzelleneinschlusse,” ‘‘Vir- chow’s Archiv,” 1892, Bd. cxxvu. 207. Virchow, “ Krankhafte Geschwiilste,” 1. 208. Volkmann, R., “ Beitrage zur Chirurgie,” Leipzig, 1875, un d “Deutsche Zeitschr. f. Chirurgie,” 1880, Bd. xm. 209. Waldeyer, “ Volkmann’s Sammlung klin. Vortrage,” I, No. 13. 210. Walker, J. W., “A Case of Pyloric Carcinoma and Melancholia, with Internal Illusions,” “ Amer. Jour. Insan.,” 1897, liii, 510-512. 21 1. Wazoldt, “Ueber einen Fall von Absonderung eines iibermassig sauren Magensaftes bei Magencarcinom,” “ Charite Annalen,” 1888, XIV. 212. Weber, W. C., “Early Diagnosis of Carcinoma of the Stomach by Means of Chemical Analysis of the Gastric Contents,” “Jour. Amer. Med. Assoc.,” 11, vii, 1896. 213. Welch, Wm. H., “American System of Medicine,” vol. 11, “ Cancer of the Stomach,” p. 53, no references. 214. West, Charlotte C., “ Report of Two Cases of Cancer of the Stomach,” “ Phila. Polyclin.,” 1898, vii, 107-110. 215. Willigk, “ Prager Vierteljahresschrift,” vol. x, 2, 1853. 216. Winterberg, J., “ Zwei Falle von Magencarcinom mit Perforation durch die vordere Bauchwand,” “Wien. klin. Rundschau,” 1898, xn, 585, 607. 217. Witte, W. C. F., “ Carcinoma of the Stomach, Retrogressive Lymphatic Transport, Multiple Carcinomatous Construction of the Ileum, and Triple Simultaneous Perforation,” “ Phila. Med. Jour.,” 1898, I, 846-848. 218. Witzel, “ Centralbl. f. Chirurg.,” 1891, No. 31. 219. Worthington, N., “ Cancer of the Stomach,” “Montreal Med. Jour.,” 1897-98, xxvi, 601. 220. Wortmann, Carl, “Ein Fall von Carcinoma ventriculi im Anschluss an chronisches Magengeschwiir,” Dissert., Wurzburg, i896-’97. 221. Wyss, “Blatter f. Gesundheitspflege,” Zurich, 1872-74. 222. Yates, H. W., “ Cancer of the Stomach, with Report of a Case,” “ Phys. and Surg.,” Detroit and Ann Arbor, 1898, xx, 147— 1 55 ; Discus- sion, 179. TABLE OF DIFFERENTIAL DIAGNOSTIC POINTS. TABLE OF DIFFERENTIAL DIAGNOSTIC POINTS. — (' 588 ■ a o rail's £-l r __, 0J - c S C u a rrt S 1 g a o U A 2 o i: 11 a s ^5 Hi : a £ ) a* a g .2- a aj i * 3 ' g*° O^d S a « bfl'-S o § 2 X .§ ^ o5 ^ 2 &*■£ o^.S 3 2 Sg**- -o "X •£ a 2 ~ b/3 n 6 « s ^ a, c 3 b/> 'U. 2 a a^- -oT°a : *■* « g s s !<§ cj a a X o a 2 ^ t 3 a .0 g o a, IBS' X MS >> a a § I § -S -9 589 590 STOMACH DISEASES CAUSED BY INFECTIOUS GRANULOMATA. CHAPTER V. STOMACH DISEASES CAUSED BY INFECTIOUS GRANULOMATA. These affections have, almost exclusively, a purely pathological significance. Among the infectious granulations reported as affect- ing the stomach are tuberculosis, syphilis, abdominal typhus, glanders, and lymphadenoma. We shall consider gastric tubercu- losis and syphilis separately. Typhoid neoplasms and ulcerations of the stomach are very rare; even more unusual than tuberculous ulcerations. The medullary swelling of lymph-glands, however, as well as the ulcers arising therefrom, have been described as occurring in the stomach (Orth, “ Specielle pathol. Anatomie,” Bd. i, S. 714). Concerning the occurrence of glanders in the human stomach, only one observation is on record — viz., Bollinger (O. Wyss), “ Rotz,” “von Ziemssen’s Handb.,” Bd. in, S. 482, 1876. Leukemic and aleukemic lymphadenomata, as occurring in the human stomach, have been reported several times (“ Lymphade- noma, “ Cornil and Ranvier, “ Manuel de l’Histolog. Patholog.,” p. 294). This neoplasm occurs in the deeper part of the true mucosa and in the submucosa, but sends prolongations into the outer layers. Lymphadenomata and glanders may ulcerate on the inner surface of the stomach. TUBERCULOSIS OF THE STOMACH. The gastric mucosa has almost entire immunity from bacterial in- fection. As the intestines are the seat of frequent infection, when there can be no doubt that bacteria have entered through the esopha- gus and stomach, the immunity of the last-named organ must depend upon some peculiarity in its structure or secretions. Tubercle bacilli are not affected by the acid gastric juice, as has been proved by Falk (loc. cit .) and Frank (loc. cit .), who demonstrated that the growth of the bacilli could not be retarded by the gastric secre- tion. This does not imply, however, that these bacilli can grow in the gastric juice. The normal stomach, as a matter of fact, is not favorable to bacterial development. The gastric immunity may further be accounted for by the scarcity of lymph-glands in the TUBERCULOSIS OF TIIE STOMACH. 5QI gastric wall. In the intestines 'lymphatic nodules are abundant, and they bear some definite relation to the formation of tubercle. The occurrence of smaller and larger tuberculous foci in the stomachs of adults and children proves that the gastric immunity can not be complete. Undoubtedly a number of conditions must simultaneously cooperate to bring about a tuberculous invasion. Prominent among these are : (1) A lessened resistance or reduced vitality of the gastric mucous membrane ; (2) a diminished secre- tion or absence of HC 1 ; (3) an altered state of the blood ; (4) the presence of tubercle bacilli. A number of the tuberculous gastric ulcerations that are reported have developed, not from a direct invasion of the bacilli into the mucosa, but from an invasion into the serosa, occurring from circumscribed or diffuse peritonitis. Gastric tuberculosis occurs in two forms — (1) miliary tuberculosis of the wall of the stomach, a not uncommon type; (2) tubercu- lous ulceration of the stomach, an extremely rare occurrence. Miliary tuberculosis of the stomach occurs simultaneously with the eruption of tubercle throughout the organism. It is usually found to exist with a miliary tuberculosis of the intestines and peritoneum. These cases may strongly resemble severe attacks of typhoid fever. The author, while physician-in-charge of Bay View Asylum, Bal- timore, observed two cases of acute miliary tuberculosis which were diagnosed as typhoid fever. Even the characteristic rose spots were present, and taken for such by the author and other clinicians. This was at a time when microscopical examination for tubercle bacilli was not in vogue, and the Widal test not yet discovered. The necropsies were made by Professor William T. Councilman, revealing acute miliary tuberculosis. The immunity of the stomach from tuberculosis was shown in the experiments of Orth (loc. cit.). By feeding rabbits with tubercle bacilli he obtained intestinal tuberculosis seven times, and gastric tuberculosis but once. In a case of tuberculosis of the esophagus reported by Dr. S. Flexner (loc. cit.), although extensive destruc- tion of the esophagus existed, and the pleural cavity had been opened, and though millions of tubercle bacilli must have been taken into the stomach, this observer assured us that no gastric tuberculosis was detected. Clinically, gastric tuberculosis is without much significance. It is, as a rule, not diagnosticated. Tuberculous ulcerations are found most frequently in the pyloric part, and Orth describes isolated 592 STOMACH DISEASES CAUSED BY INFECTIOUS GRANULOMATA. miliary tubercles occurring in the vicinity of ulcerations. In rare cases tuberculous ulcerations have produced fatal symptoms by disintegrating and eroding a gastric artery, or by perforating the gastric wall. The demonstration of the tubercle bacillus in a gastric ulcer was first made by Coats {loc. cit .). Matthieu and Remond {loc. cit.), Musser {loc. cit), and Serafini {loc. cit.), in their cases, also succeeded in proving the presence of tubercle bacilli. Kiihl examined for the tubercle bacillus in four cases from the Pathological Museum of the University of Kiel, but could demon- strate it positively in only two of these, which were recent cases. The other two were older specimens, having been in the museum a long time. A large number of the reported cases of tubercular ulcers are doubtful,' either because no microscopic examination was made at all, or the authors failed to stain for the bacillus. Such cases are those of Paulicky {loc. cit.), Hebb {loc. cit), Chvostek {loc. cit., four cases), Lange (loc. cit), Barlow (loc. cit), Quenu (loc. cit), and Bignon. The earliest reported case of tubercular ulcer is Litten’s (loc. cit), which showed an isolated ulcer on the anterior gastric wall, with typical giant cells and caseating tubercles. Letorey (loc. cit) recently reported a case, and gave an analysis of 21 cases. In 1887 Marfan reviewed the subject, and collected 14 authenticated cases. The disease is most frequently found in males. In 19 cases collected by Letorey, in which the sex was stated, it occurred 16 times in males and 3 times in females. The ulcers are usually single. In a case from Professor Osier’s clinic, however, at the Johns Hopkins Hospital (parts of this stomach were presented to the author for examination through the kindness of Dr. S. Flexner, who performed the autopsy), there were numer- ous ulcers of various sizes. In this case the intestines were also the seat of numerous ulcerations penetrating to the muscular coat. The stomach showed 118 to 120 areas of loss of substance over the entire organ, but most thickly on the anterior surface near the greater curvature. Hermann Durck (loc. cit) observed four cases of undoubted tuberculous ulcer in 900 autopsies at Munich. Frerichs and Litten have reported cases in which the a tuberculous ulceration was limited to the stomach, the intestines being intact. The sizes of the ulcers vary from a pin’s head to five centimeters in diameter. Musser (loc. cit) has reported a case of a tuberculous ulcer 1x3 inches in extent ; and in one of the cases of Durck (loc. cit), occurring in a child ten years old, there existed an ulcer exceeding in size that of a German five-mark piece (somewhat TUBERCULOSIS OF THE STOMACH. 593 larger than a silver dollar). Secondary tuberculous changes may extend to the stomach through perforation resulting from caseat- ing neighboring lymph-glands. This is generally rapidly followed by purulent processes in the glands. When the peritoneum of the stomach becomes involved in a general peritoneal tuberculosis, the posterior wall of the organ, which is probably the most protected, is either entirely free, or, at any rate, is much less affected than the anterior wall. Habershon {loc. cit.) assumes that infection of the gastric mucosa occurs by way of the vascular channels. He does not believe in a direct infection of the mucosa because of the acidity of the gastric juice. Klebs (“ Tuberculose,” published by Leopold Voss, 1894, p. 80) assumes that tuberculous new formations occur on the basis of preexisting gastric ulcers. A critical review of the literature is given in an interesting report of multiple tuberculous ulcers of the stomach (three cases, by Alice Hamilton, M.D., “ Johns Hopkins Hospital Bulletin,” April, 1897). The bibliography, though extensive, is not quite complete, and we have, in the following, added cases which have come to our notice. In these three cases tubercle bacilli were demonstrated by the Ziehl-Neelsen method of staining. Dr. Hamilton inclines to the opinion of Klebs, that gastric erosions, or previously existing losses of substance, constitute the portals of entry for the tubercle bacillus. The facts in the second case indicate that many small erosions of hemorrhagic origin preexisted in the stomach, some of which became invaded with tubercle bacilli swallowed with the sputum. Perforation not infrequently occurs. It was present six times in the fourteen cases reported by Marfan — three times through a tuberculous gland’. In eight of Letorey’s cases the presence of a gastric tuberculosis was suspected during life and confirmed at the necropsy. Death by perforation peritonitis resulted in a case re- ported by Paulicky (loc. cit.). Most frequently death results from advanced tuberculosis in other organs. In three of the cases death was caused by severe hemorrhage following an erosion of a blood-vessel through the ulcerative process. In the critical con- sideration of the subject by Dr. Hamilton ( loc . cit.) it was found that the authentic literature contained fifteen undoubted cases, and nine more, which were probable, but not proved. While there is a disposition for development of tuberculosis in the intestine, there are numerous cases reported where ulcers existed in the stomach, the intestines being wholly exempt. The deepest ulcers, 39 594 STOMACH DISEASES CAUSED BY INFECTIOUS GRANULOMATA. when found multiple in the stomach, do not extend beyond the muscularis mucosae, and the infiltration of the mucous membrane extends little further than the actual ulceration. These facts are very evident in the sections kindly presented to the author by Dr. S. Flexner, and which were taken from the cases reported by Dr. Hamilton. Superficial small ulcerations still showed vestiges of glands, but without any recognizable distinction between oxyn- tic and chief cells. Epithelioid and lymphoid cells were pro- fusely scattered throughout the remnants of mucous membrane. The free surfaces of the ulcers were in a state of necrosis, covered at times by a homogeneous, finely granular matter. The deeper layers were in a state of comparative preservation. Tubercle bacilli were present in small numbers, both on the free surface of the ulcers and among the remnants of the glands. Letulle (Anatom. Societe Paris, 1893; also abstracted in “ Centralbl. f. allgem. Pathologie,” Bd. iv, 1893, S. 760) in 108 autopsies on undoubted cases of pul- monary tuberculosis, found but one case of tuberculosis of the stomach. The organ presented ten submucous nodules as large as peas, containing giant cells and a few tubercle bacilli. Diagnosis. — The diagnosis of the possible tuberculous nature of a gastric ulcer during life is certainly very problematical. Tubercle bacilli that may be found in the gastric contents do not serve to throw light on the subject. They may have been swal- lowed, or they may have been contained in the food. The only possibility would be to use a weak hypodermic injection of tuber- culin (one milligram), and if a temperature reaction follows when all signs of tuberculosis in the lungs, larynx, and other organs are absent, then the diagnosis of a local tubercular ulcer in the stomach would be justifiable. J. Petruschky (“ Verhandlungen d. XVI. Con- gress. f. innere Medicin,” April, 1899, S. 366) reports two cases with the typical clinical history of gastric ulcer that did not im- prove after the most approved treatment for this disease. An injection of one milligram of tuberculin was followed in five days by five milligrams, and in six days by ten milligrams. After the third injection a violent reaction set in, particularly an intense local reaction of the stomach, expressing itself in vomiting (without blood) and gastralgic pains. There were no reactions on the part of the lungs or other organs. After every injection an increased sensitiveness of the gastric region was evident. The diet consisted mainly of milk, and no internal medication was given. The general condition and strength of the patient improved visibly. Toward LITERATURE ON GASTRIC TUBERCULOSIS. 595 the end of the treatment the patient received injections containing ioo milligrams. Recovery was complete after three months. The first case continued well without a relapse for five years. The cure of the second case was not complete at date of report. This author states that the test-meals from these cases, a half-hour after an Ewald test-breakfast, showed a distinct reaction for free HC1. This evidence might be useful in the rare cases where tubercular ulcer might be confounded with carcinoma. LITERATURE ON GASTRIC TUBERCULOSIS. 1. Anger, in Marfan’s “ Thesis,” Paris, 1887. 2. Barbacci, “ Lo Sperimentale,” May, 1890. 3. Barlow, Path. Soc., London, 1887. 4. Beadles, “ British Med. Jour.,” 1892, 11. 5. Bellrose, N. W., “ Gastric Ulcer, Probably Tubercular, Report of a Case,” 44 Colorado Med. Jour.,” 1897, in. 6. Birch-Hirschfeld, “ Lehrbuch d. path. Anat.,” Bd. ii, S. 642. 7. Bias, “Ueber tuberculose Geschwiire des Magens,” Dissert., Munchen, 1895-96. 8. Blumer, G., “ Tuberculosis of the Stomach, with a Report of a Case of Multiple Tuberculous Ulcers of that Organ,” “ Albany Med. Ann.,” 1898, xix. 9. Brechemin, “ Proge’s Medical,” 1879. 10. Cazin, in Fernet’s article, “Bull, et Mem. d. 1 . Soc. Med. des Hop.,” 1880, tome xvii. 11. Chvostek, “Wien. med. Blatter,” 1882, v. 12. Coats, “Glasgow Med. Jour.,” 1886. 13. Cordua, “ Arbeiten aus dem patholog. Institut in Gottingen,” Berlin, 1893. 14. Duguet, in Spillman’s “These,” Paris, 1878. 15. Diirck, Hermann, “ Ergeb. d. allgem. Path.” (Four Cases of Tubercu- lous Ulcer in Nine Hundred Autopsies). 16. Eppinger, “ Prager med. Wochenschr.,” 1881. 1 7. Falk, “Virchow’s Archiv,” Bd. xciii, S. 177. 18. Flexner, S., “ Tuberculosis of Esophagus,” “Bull. Johns Hop. Hosp.,” No. 28, 1893. 19. Frank, “ Deutsche med. Wochenschr.,” 1884, No. 20. 20. Habershon, S. H., “ Trans. Path. Soc.,” London, vol. xlv, p. 7 3. 21. Hamilton, Alice, “Johns Hopkins Hospit. Bulletin,” April, 1897. 22. Hattute, “ Gaz. des Hop.,” 1874. 23. Hebb, G., “ Westminster Hosp. Reports,” 1888, ill. 24. Kanzow, “ Ein Beitrag zur Casuistik der tuberculosen Magenge- schwiire,” Dissert., Munchen, 1893-96. 25. Kuhl, “ Thesis,” Kiel, 1889. 26. Labadie-Lagrave, “ Bull. Soc. Anat.,” 1870. 27. Lange, “ Memorabilien,” Heilbronn, 1871, XVI. 28. Lava, “ Gazz. Med. di Forino,” 1893. 59 6 STOMACH DISEASES CAUSED BY INFECTIOUS GRANULOMATA. 29. Letorey, “These,” Paris, 1895. 30. Litten, “ Virchow’s Archiv,” 1876. 31. Lorey, “ Bull. d. 1.. Soc. Anat.,” 1874. 32. “ Lubarsch und Ostertag,” vol. 11, p. 336. 33. Marfan, “ These,” Paris, 1887. 34. Mathieu and Remond, in Letorey’s “ Thesis,” Paris, 1875. 35. Mathieu, “ Bull. d. 1. Soc. Anat.,” 1881. 36. Muller, K., “ Ueber Dyspepsia praetuberculosa,” “ Ungar. med. Presse,” Budapest, 1898, ill. 37. Miisser, “ Phila. Hosp. Reports,” 1890, 1. 38. Oppolzer, in Marfan’s “ These,” Paris, 1887. 39. Orth, “ Exper. Magengeschw.,” “Virchow’s Archiv,” Bd. lxxvi. 40. Packard, F. A., “ Tuberculous Ulcer of the Stomach,” “ Tr. Path. Soc.,” Phila., 1898, xviii. 41. Paulicky, “Berlin, klin. Wochenschr.,” 1867. 42. Pozzi, “ Bull. Soc. Anat.,” 1868. 43. Prezewoski, “Gastritis Tuberculosa” (five cases), “ Centralbl. f. allgem. Path. u. path. Anat.,” Bd. vi, S. 270. 44. Quenu, in Marfan’s “ Thesis,” Paris, 1887. 45. Serafini, “ Annal. clin. del Osp. di Napoli,” 1888. 46. Talamon, “ Progres Med.,” 1879. 47. Weinberg, “Ulceration Tuberculeuse de l’estomac,” “Soc. Anat. de Paris,” 5, vi, 1897. 48. Wilms, M., “ Miliar tuberculose des Magens,” “ Centralbl. f. allg. Path, u. path. Anat.,” Jena, 1897, vui. 49. Petruschky,“ Verhandlung. d. XVI. Congress, fur innere Medicin,” Wies- baden, April, 1899. SYPHILIS OF THE STOMACH. Pathological changes caused by syphilis occur in the stomach in two main forms — (1) the syphilitic ulcer and (2) the syphilitic neo- plasms. In addition to these the author recognizes a third form — (3) the diffuse syphilitic gastritis (chronic form). While the first two forms are due to direct syphilitic disease, the third form may be due to indirect syphilis — for instance, to the formation of countless syphilitic gummata, forming nodules in the mucosa and submucosa barely visible to the naked eye. This third form, in the majority of cases, is probably due to what Chiari terms indirect syphilis — that is, due to circulatory disturbances, passive congestions, hemorrhages, etc., produced by syphilitic disease of other organs, especially of the liver. Gastric disturbances are observed in individuals affected with syphilis, even at an early prodromal stage of cutaneous eruptions. These patients may develop all the symptoms of acute gastritis, with a feeling of pressure, fullness in the stomach, loss of appetite, PLATE IX. mm «V» A' # • %. y* i* (c , ~ A >; V tssafc Bj j g MS ■ :;V 5f.& J s& • ; 'ifxgMfe ♦•^a•»•»«*•***• zm®ste: SYPHILIS OF THE STOMACH. 597 nausea, etc. The symptoms of acute or subacute gastritis may be accompanied by gastralgia, coated tongue, headache, and actual vomiting. These symptoms can not be pronounced as syphilitic, because other etiological factors can not be excluded ; one is there- fore disposed to assign the gastric symptoms to better known causes. Allen A. Jones has reported two cases of gastralgia, which were undoubtedly caused by syphilis (“ Phila. Med. Jour.,” vol. hi, p. 958). Acute diseases of the neighboring organs (liver, pancreas, and spleen) are not so rare in syphilis as was assumed not long ago. Jullien {loc. cit.) describes attacks of vomiting, colic, and diarrhea in the course of recent syphilis; and, according to Fournier {loc. cit), bulimia is, in rare cases, a symptom in severe forms of lues. This condition is observed more frequently in women than in men, and occurs between the third and sixth month of the disease. According to this author, it is sometimes associated with polydipsia. In a consideration of the previous gastric diseases we have seen that the nerves react in a very sensi- tive manner to certain anomalous states of the blood — anemias, etc. In lues we have characteristic reduction of the erythrocytes and of the percentage of hemoglobin. We might trace the symp- toms described to these blood conditions in preference to ascribing them to disease of the gastric mucosa. Chronic Gastritis Due to Syphilis. — This is a rather frequent and important syphilitic affection, and is one of the main causes of the poor state of nutrition in luetics. It is, as a rule, associated with characteristic syphilitic disease in other digestive organs (spleen, pancreas, and liver). Histologically, it may be found to be a simple chronic gastritis, or else combined with gummata or gummatous ulcers, and is then a phenomenon of the later stages. Syphilitic chronic gastritis, in the absence of gummata or gum- matous ulcers, does not differ pathologically from ordinary chronic gastritis, except in the greater frequency of small round- cell accumulation, especially in the submucosa, sometimes appearing like miliary gummata. The cases that are described by Virchow {loc. cit) were due to chronic passive hyperemia caused by circu- latory disturbances, and, in our opinion, present nothing character- istic of syphilitic gastritis. Chronic syphilitic gastritis may develop from repeated attacks of the acute form, just as with non-specific chronic gastritis. Relapses are not necessarily due to syphilis. If characteristic syphilitic lesions exist in the liver, kidneys, 598 STOMACH DISEASES CAUSED BY INFECTIOUS GRANULOMATA. spleen, pancreas, or intestines, the chronic gastritis should, in my opinion, be attributed to syphilis. In tertiary syphilis the remark- able malnutrition is due to a chronic luetic gastritis. The clinical phenomena of luetic gastritis are not different from the non-specific inflammations of the stomach. Diagnosis . — It is conceded by gastro-enterologists that iodids and salts of mercury have a deleterious effect upon the gastric functions in normal individuals. If, therefore, the symptoms of gastritis develop in a confirmed luetic, and improve upon the administration of iodid of mercury, getting worse when the mer- cury is discontinued and improving again when the drug is re- sumed, the diagnosis of chronic syphilitic gastritis is logical. We have observed symptoms of acute gastritis in a child eleven years old, daughter of a man who had contracted syphilis while he was a soldier in the German army in the Franco-Prussian war, i 870 -’ 7 I. The father of this child has had maniacal attacks, in which he had to be restrained. About once a month he has typical epileptic convulsions, which may last, with short intervals, for ten to twelve hours, with foaming at the mouth, involuntary evacuations, etc. He admits the original infection, and gives a correct history of primary and secondary syphilis. The child recently developed a huge gumma of the lower jaw, which assumed the dimensions of a goiter. The gastric symptoms were incessant vomiting and gas- tralgia. By treatment with mercurial inunctions the stomach symptoms disappeared in the course of two weeks ; the child was apparently cured after six weeks of this treatment. The efficacy of this form of treatment was all the more fortunate since the child could retain nothing on its stomach and medication by the mouth would have been futile. Two years ago the author treated another child of this man (his wife, by the way, has had four miscarriages), for gastralgia, nausea, eructations, and vomiting, by mercurial inunc- tions and a saturated solution of iodid of potassium. The child took as much as forty drops of the saturated solution of KI three times a day, with evidences of distinct improvement, the symptoms subsiding entirely at the end of three weeks. In both of these children the vomit during the attacks contained no free HCl,but enormous quantities of mucus, and curdled milk but weakly. Both HC1 and ferment secretion were restored by the treatment. Tullio (loc. cit) reports improvement and cure of severe chronic gastritis by iodid of mer- cury given internally. The patient became worse when the mercury was discontinued. Non-syphilitics were made dyspeptic by taking HISTOLOGY OF SYPHILITIC GASTRITIS. 599 iodid of mercury. The following conclusions appear to us to be logical. When digestive disturbances resembling those of gastritis occur in a syphilitic, and other etiological factors can be excluded, the diagnosis of syphilitic gastritis is correct if the phenomena dis- appear under antisyphilitic treatment. The diagnosis, then, depends upon the evidence of undeniable syphilis as a cause, and the disap- pearance of gastric symptoms under antisyphilitic treatment. Pro- fessor S. Flexner (pathologist to the Johns Hopkins Hospital) pre- sented us with the stomach of a syphilitic negro who had gummata in the following places: (i) Frontal bone, extending into the men- inges and frontal cerebral convolutions ; (2) one in the liver ; (3) one in the spleen ; (4) three in mesenteric glands ; (5) one in the testes and epididymis. The author was present at the autopsy, which was made by Dr. Flexner. After hardening in formol, the sections were stained in orange-G. and hematoxylin. All the sections, no matter from what portion of the stomach they were taken, showed an intense diffuse gastritis. At first we failed to find characteristic evidence of lues. The surface of the mucosa was covered with finely granular elevations, quite evident to the naked eye. The surface cylindrical epithelium was lost entirely. There was a very characteristic endarteritis and thickening of the vessel walls, pro- ducing occlusion of the lumen (endarteritis obliterans). Through- out the mucosa and submucosa were countless miliary nodules, about the size of a pin’s head, composed of apparently densely packed collections of small round cells. Some of these nodules exhibited themselves in the submucosa, but in that situation they were rare. The majority of them rested upon the muscularis mucosae, and thence extended upward into the glandular layer, pushing apart, compressing, and distorting what was left of the gland ducts. Some of the small round-cell infiltrations resem- bled normal lymph-glands of the stomach. The majority of them were, however, larger than the gastric lymph-glands, extending from the submucosa to the surface of the mucous membrane. (See illustration, plate IX.) One of our artists (Mr. Louis Schmidt) has given a graphic illustration of the condition present. In many places collections of round cells had forced asunder the fibers of the muscularis mucosae, splitting apart this layer, which usually runs along in one stratum. In some places the muscularis mucosae was seemingly torn apart and forced either downward into the submucosa, or upward into the mucosa, in large bundles, by infiltrating masses of round cells and also by proliferation of 600 STOMACH DISEASES CAUSED BY INFECTIOUS GRANULOMATA. the muscle-fibers. The longitudinal layer of muscle-fibers was similarly split up by enormous collections of round-cell infil- tration. The fibers of the muscularis mucosae normally as- cend into the glandular layer and surround the gland tubules. We have, however, never seen these muscle-fibers ascending in such masses as in these specimens. In places the entire glandular layer was replaced by a mass of small round cells. The left side of the illustration represents one of the miliary nodules, showing a gradual breaking down or softening at the side. Although at first inclined to consider this whole process due to indirect syphilis, caused by passive congestion due to the luetic hepatitis (a large gumma being present in the liver), the finding of nodules as large as a pin’s head (which showed signs of softening) suggests that we may possibly be dealing with minute miliary gummata. Chiari ( loc . cit.) reported 243 autopsies of undoubted syphilitics : 145 were hereditary and 98 acquired syphilis. His conclusions are the fol- lowing : (1) Pathological changes caused by syphilis really occur in the stomach ; (2) they may be direct syphilitic changes, or owe their origin indirectly to syphilis ; (3) the direct syphilis of the stom- ach is a great rarity, and is either a gummatous process or a simple inflammatory infiltration; the latter occurs only in the hereditary form ; (4) the indirect syphilitic affections of the stomach are due to circulatory disturbances caused by syphilis of the other organs, especially of the liver, or else they are due to gastric hemorrhages occurring interstitially as phenomena of a syphilitic hemorrhagic diathesis ; (5) gummatous processes in the stomach are character- ized by presence of gummatous tissues ; they are first developed in the submucosa, and enter the other layers from there ; (6) syphilitic gastric ulcers may be caused by disintegration and autodigestion. The cicatrices in the stomach demonstrated by Cornil {loc. cit.) and Weichselbaum (loc. cit.) could be attributed to syphilis only if gummatous tissue or other non-ulcerating gummata were present. Only in three cases could Chiari designate the changes as direct syphilis — one gumma in a case of hereditary syphilis, one gumma in a case of acquired syphilis, and one in diffuse inflammatory infiltration of the mucosa and submucosa in hereditary syphilis. His percentage of gastric syphilis was 1.2 per cent, of the total material of 243 sections: 1.3 per cent, in hereditary syphilis, and 1.2 per cent, of acquired syphilis. Syphilitic Ulcers of the Stomach. — In a study of the sub- joined literature authentic cases of syphilitic gastric ulcers are not GASTRIC ULCER RESULTING FROM SYPHILIS. 601 so scarce as one might presume. Galliard ( loc . cit.) and Cruveilhier ( loc . cit.) were disposed to believe in a causative relation between simple gastric ulcer and syphilis. Among one hundred cases of gastric ulcer, Engel could trace a syphilitic history in ten per cent. T. Lang (loc. cit.) stated that twenty per cent, of gastric ulcers occur in syphilis. Ewald expresses himself with doubt on this subject: “ It must remain questionable,” he says, “ in two diseases as common as those under discussion, whether we are dealing with cause and effect, or with accidental coincidents.” Frerichs, Drozda, Murchison, and Chvostek found scars in the stomach, coincidently with general syphilis. Gastric ulcers may occur in syphilitics from necrosis of the mucosa, due to specific endarteritis, or to disintegration and breaking down of a gumma. In 1838 Andral (loc. cit.) concluded that a gastric ulcer in his clinic was due to syphilis because it was cured by mercurial treatment. Rosanow (loc. cit.) described a case in a soldier who had suffered from gastric ulcer for eight years and had been treated by him for two months by typical ulcer treatment. The cardialgia, however, continued, and was associated with pains in the lower extremities. The patient showed no signs of lues. He was cured in forty-seven days by treatment by inunctions and iodid of potassium. It is necessary to distinguish between typical simple round ulcers occurring in syphilitics, and gummatous ulcerations, with gastritis. According to Wagner (loc. cit.) and Klebs (loc. cit.), all ulcers found in the stomachs of syphilitics have arisen from gummata, but Galliard (loc. cit.), Lang (loc. cit.), and Mauriac (loc. cit.) differ from this opinion, and hold that the syphilitic gastric ulcers do not necessarily arise from gummata. T. Lang’s (loc. citi) statistics indicate that twenty per cent, of gastric ulcers occur in luetic subjects, and Neumann (loc. cit.) asserts that syphilis is more often the cause of gastric ulcer than has been hitherto believed ; furthermore, that gastric ulcers occurring in syphilis do not develop from gummata, but have the same manifold etiology as the non-specific ulcer. They may develop from erosions, which are very frequent in syphili- tics ; from endarteritis ; from diminution in the amount of hemo- globin; and from reduction of the alkalinity of the blood, increase and disintegration of the leukocytes. These states are character- istic of lues, and are accepted as etiological factors of round ulcers also. To these might be added hyperacidity and bacterial in- fection causing necrosis. In a case of Fauvel’s (loc. cit.) the stomach showed chronic gastritis and several ulcers. In a case of Capozzi’s 602 stomach diseases caused by infectious granulomata. (loc. cit .) numerous ulcerations of the mucosa extended from the cardia along the greater curvature to the pylorus. In a case of Oser’s the patient was affected with a syphilitic papulous eruption and psoriasis palmaris, the gastric mucosa was injected and per- meated by numerous hemorrhagic erosions. The symptoms, course, and termination of syphilitic gastric ulcers are not different from the non-syphilitic. In a case of Rosanow’s (loc. cit.) the gastralgia occurred only at night, and from this the author diagnosticated the probable syphilitic nature of the ulcer. Bartumeus (loc. cit.) speaks of nightly vomiting occurring with syphilitic ulcer. Diagnosis. — When other etiological factors — such as tuberculo- sis, alcoholism, chlorosis, and the manifold causes which have been enumerated in the article on ulcer — can be excluded, and undoubted syphilis can be established, the diagnosis of the syphilitic origin of gastric ulcer might be made, although not with certainty. The diagnoses of Andral (loc. cit), Hayem (loc. cit), and Mark (loc. cit) were based upon the curative effect of antisyphilitic treatment. Prognosis. — Wagner (loc. cit), Lanceraux, and others, report cures of syphilitic ulcers by iodid^of potassium. The conditions after the reported cures were similar to those existing after the cures of non- specific ulcers. Stenosis of the pylorus and chronic gastritis fol- lowing syphilitic ulcers have been observed by Cornil, Capozzi, Wagner, Fauvel, and Klebs. The direct cause of death in autopsies of cases of syphilitic gastric ulcers hitherto reported was plainly attributable to pathological states in other organs, such as tuber- culosis, amyloid and fatty degeneration of various viscera, dropsies, and edema. Some of the cases reported as syphilitic are doubtful. This is my opinion of the case reported by Zavadski and Luxen- bourg (loc. cit), in which no characteristic syphilitic lesions are described, for the endarteritis and the small round-cell infiltration may occur in chronic gastritis of a non-luetic character. The patient, a medical student, had denied luetic infection. Syphilitic Neoplasms of the Stomach. — The percentage of gastric gummata occurring in syphilis has already been stated in the results given from 243 autopsies on syphilitics performed by Chiari (loc. cit). Gastric gummata have been described by Galliard (loc. cit), Cornil (loc. cit), Birch-Hirschfeld (loc.. cit), Chiari (loc. cit), Wagner (loc. cit), Klebs (loc. cit), and Lanceraux (loc. cit). Cornil’s case, which may be regarded as typical, was that of a woman who had gummata both in the liver and stomach. That in the stomach SYPHILITIC NEOPLASMS. 603 was located on the lesser curvature, and had the appearance of a flattened reddish tumor, two to five centimeters in diameter. The gastric gummata reported by Chiari (loc. cit .) were sharply circum- scribed elevated swellings. They occur together with gastric or intestinal ulcers or cicatrices, and develop in the submucous layer as dense, compact, felt-like masses, formed of fasciculi of con- nective tissue infiltrated with small round cells. From the sub- mucosa they advance into the serosa and mucosa. The mucosa is thickened, smooth, and glistening, and of a pale yellow color. The muscularis and the serosa are also thickened. The condition of the gummata will vary with the stage in which they are found. In one case Cornil found three gummata — respectively two, three, and five centimeters in diameter — in the neighborhood of the pylorus. The mucosa over these gummata was thinned out and adherent. Lanceraux (loc. cit) found an ulceration thirty centi- meters in diameter in close proximity to the pylorus on the lesser curvature. The case was that of a man sixty-six years old, with many manifestations of syphilis. The ulceration had destroyed the gastric wall — thinned it down to a very delicate lamella. The nodule was in a state of fatty disintegration, and apparently had prevented a perforation by its own structure. Birch-Hirschfeld’s case occurred in a new-born infant, with skin syphilis and a gumma in the liver and lungs. In the pylorus was a slightly elevated thick area, as large as the palm of the hand. It was of a whitish color and of tolerably firm consistence, formed of granulation tissues infiltrated with masses of small round cells. Weichselbaum (loc. cit.) described two ulcers and one cicatrix at a spot where the transition of the fundus into the pyloric part occurs. One of the ulcers had a triangular shape and was twelve millimeters long. This occurred in a man twenty-five years old, with syphilitic mani- festations of the cranium, nose, throat, larynx, and liver. Another case of Chiari’s, a child three weeks old, with pemphigus syphiliti- cus, swelling of the inguinal glands, and fissures in the lips, tongue, and penis, showed in the lungs numerous nodules as large as peas, some as large as hazelnuts. There was an induration in the hilus of the liver, and a similar callosity on the common bile-duct, and also on the cystic duct. The wall of the gall-bladder neck was strongly infiltrated. The gastric mucosa showed five plate-like gummata. The gastric gummata generally soften, break down, and ulcerate ; this has been the cause of assigning all syphilitic ulcers to the breaking down of gummata. The ulcer which arises from a 604 stomach diseases caused by infectious granulomata. gumma is a loss of substance that is smaller in the true mucosa than in the submucosa. The simple perforating gastric ulcer is a loss of substance that is greatest in the true mucosa, becomes smaller in tjie submucosa, and still smaller in the muscularis. This gives the simple gastric ulcer the characteristic terraced appearance, which is never seen with a gummatous gastric ulcer. The edge of the simple gastric ulcer is not undermined, but has the appearance as if cut out with a punch. The edge of the gummatous gastric ulcer, however, is irregular, angular, rolled up, and often undermined. The surroundings, the walls, and the floor of the simple gastric ulcer exhibit no pus and no necrotic tissue elements ; perhaps some slight hemorrhagic infiltration is observa- ble, if a previous hemorrhage has occurred. The gummatous gas- tric ulcer is covered by a yellow, tough, gelatinous deposit. In the surroundings one frequently finds gummata. Old and extensive simple ulcers may closely resemble gummatous ulcers on account of the fibrous thickening of the edges. The occurrence of gum- mata in other parts of the digestive tract or organs may then decide the nature of the gastric neoplasm. Gummata of the stom- ach, according to Neumann, are manifestations of late lues. The cases of Birch-Hirschfeld (Joe. cit.) and Chiari (loc. cit .), however, were inherited syphilis. Diagnosis. — These lesions do not give symptoms sufficiently characteristic to make their clinical recognition possible. In pronounced syphilitics, with palpable hepatic gummata and steno- tic symptoms in the stomach, antisyphilitic treatment may possibly give some clue regarding the nature of the gastric neoplasm. Hemorrhage from the Stomach as a Result of Syphilis. — This is an extremely rare occurrence. Hayem reports a case of grave hematemesis which baffled the usual treatment, but ceased after the administration of iodid of potash. Gastric hemorrhage may occur as a result of intense passive congestion, caused by obstruction of the portal circulation. Hiller (loc. cit.) reports a case of a man thirty-nine years old, who admitted having acquired lues in 1868. In the night from the 3d to the 4th of December, 1 88 1 , he vomited large quantities of blood, and passed blood by the stool. On the 5th of December the vomiting of bright red blood was repeated ; he also had three passages that were black with partially digested blood. The gums and uvula were covered with numerous radiating scars; the pharynx showed two recent scars. In the nasal partition there was an irregular, deepened ulcer with LITERATURE ON SYPHILIS OF THE STOMACH. 605 callous edges. For several months there had been a purulent offensive discharge from the nose. There was decided enlarge- ment of the spleen and liver. Several uneven prominences were palpable on the surface of the liver. The diagnosis of syphilis of the liver was made, with passive congestion in the spleen and stomach. The patient recovered under antisyphilitic treatment. It is impossible to decide in these cases whether the hemorrhage comes from an ulcer, from hemorrhagic erosions, or from disease of the blood-vessels. LITERATURE ON SYPHILIS OF THE STOMACH. 1. Andral, “Clinique med.,” tome iv, 121. 2. Bartumeus, “ Gastralgia Intermittente Sifilitica Accompananda de Vomi- tos Vespertinos y Otros Accidents Especificos Dolorosos,” “ Revista de Cien- cias Med.,” Barcelona, 1878, 348. 3. Berthold’s “ Statistischer Beitrag zur Kenntniss des chronischen Magen- geschwiirs,” “ Aus den Sections-protokollen des patholog. Institutes zu Berlin,” i868-’82. Berlin, 1883; Dissertation. 4. Bittner, “ Centralbl. f. allgem. Pathologie,” Bd. v, 1894, S. 175; also “ Prag. med. Wochenschr.,” 1893, No. 48. 5. Birch-Hirschfeld, “ Lehrbuch der patholog. Anatomie,” 1885, II, 531. 6. Capozzi, 11, Morgagni, 1867, ix, 2, 89; Schmidt’s “ Jahrbiicher,” cxxxv, 41. 7. Chiari, “ Prag. med. Wochenschr.,” 1885, No. 47. 8. Chiari, “International. Beitrag z. Wissenschaft : Medicin,” Rudolf Vir- chow, gewidmet, 1891, Bd. 11. 9. Cornil, “ Lec^ons sur la Syphilis,’’ 1879, 4°6 ; and “ Manuel de l’Histolog. Patholog.,” 1882, 11, 296. 10. Dieulafoy, “ Syphilis de l’estomac,” Acad, de med., 17. Mai, 1898. 11. Dubuc, “Un cas de syphilis de l’estomac,” “Soc. de med. de Paris,” 28. Juin, 1898. 12. Fauvel, “ Bullet, de la Societe d’Anatom.,” 1858. 13. Flexner, S., “Gastric Syphilis, with the Report of a Case of Perforating Syphilitic Ulcer of the Stomach,” “Am. Jour, of the Med. Sciences,” Oct., 1898. 14. Fournier, “ Notes sur Certains Cas Curieux de Boulimie et de Polydipsie d’Origine Syphillitique,” “ Gaz. hebdomadaire de Med. et de Chirurg.,” Paris, 1871, Nos. 1 and 2 ; “ Gaz. des Hopitaux,” Paris, 1871, Nos. 109, no, 112. 15. Galliard, “ Syphilis Gastrique et Ulcere Simple del’Estomac,” “ Archiv. Generates de Medecine,” 1886, pp. 65-83. 16. Hayem, G., Hayem et Tissier, “ De la Syphilis de l’lntestin,” “ Revue de Med.,” Paris, 1889, 231. 17. Hiller, “ Monatshefte f. prakt. Dermatologie,” 1882, 1, 97 ff. 18. Von Jaksch, Cit. nach Bamberger, “ Krankheiten des chylopoetischen Systems,” “ Handb. d. spec. Pathologie u. Therapie,” von Virchow, VI, 1 Abth., 280. 6o 6 BENIGN TUMORS OF THE STOMACH. 19. Jullien, L., “ Traite Pratique des Malad. Vener.,” 1879, p. 615. 20. Klebs, “ Pathologische Anatomie,” 1869,1, 262, 263. 21. Lanceraux, “ Traite Historique et Pratique de la Syphilis,” Paris, 1873, 249. 22. Lanceraux, “ Traite de la Syphilis,” 1874, 248. 23. Lang, T., “ Zur Lehre von der Eingeweidesyphilis.” Sonderdruck der “ Wiener med. Presse,” 1885, No. 11. 24. Lang, T., “Eingeweidesyphilis,” “Wien. med. Presse,” 85, No. 11. 25. Mauriac, “ Syph. tert.,” p. 723. 26. Neumann, in “ Nothnagel’s specielle Patholog. u. Therapie,” Bd. xxm, Syphilis, S. 351. 27. Nolte, “ Ueber die Haufigkeit des Magengeschwiirs in Miinchen,” Munchen, 1883 ; Dissertation. 28. Orth, “ Lehrbuch d. speciellen pathol. Anatomie,” Berlin, 1887, 1, S. 709, 744. 29. Oser’s “ Vierteljahresschrift fur Dermatologie und Syphilis,” 1871, No. 27. 30. Rosanow, V., “ Magengeschwiir syphilitischen Ursprungs,” “ La Sem- aine Medicale,” 1890, No. 43. 31. Tullio, “ Contributo alio Studio delle Lesioni Funzionale Gastriche, per Sifilide edei coro Magri curative,” “ Polyclinica,” xv, Giugni, 1894. 32. Virchow, “ Handb. der spec. Pathol, und Ther.,” xi, 1, S. 71, 78. 33. Wagner, “ Das Syphilom,” “ Archiv der Heilkunde,” 1863, Bd. IV, 225 und 226, 369. 34. Weichselbaum, “ Bericht d. Rudolfspitals in Wien,” 1883, S. 383. 35. Zavadski and Luxembourg, “ Gaz. Lekaroka,” 1893, vol. xm, p. 1233, et seq. 36. “ Jahresbericht der k. k. Krankenanstalt Rudolf-Stiftung,” 1883, 383. 37. Flexner, Simon, “Gastric Syphilis; A Case of Perforating Syphilitic Ulcer of the Stomach,” “Am. Jour. Med. Sciences,” October, 1898. CHAPTER VI. BENIGN TUMORS OF THE STOMACH. Myomata. — Fibromata. — Lipomata. — Polypi. — Myxomata. — Papillo- mata. — Lymphadenomata. — Pedunculate Tumors. — Foreign Bodies. — Gastroliths. — Hypertrophic Stenosis of the Pylorus. The stomach may be the seat of a great diversity of tumors. A neoplasm that can be determined by palpation, however, is, as a rule, a carcinoma. Benign tumors are very rare, and their clinical history does not present any great interest. But occasionally they may become the cause of errors in diagnosis. This reason obliges POLYPI — MUCOUS POLYPI. 607 me to say a few words about them, as well as of other foreign bodies and gastroliths which are liable to occur in the stomach. Myomata, lipomata, papillomata, and lymphadenomata have been found in the stomach. In acute toxic gastritis caused by the ingestion of corrosive sublimate, calcareous masses may develop in the depths of the mucous membrane. In comparing simple chronic gastritis with gastric tuberculosis we have shown that in the former the glands were capable of undergoing a cystic degeneration more or less pro- nounced. Aneurysms of vessels in the walls of the stomach have also been described. Polypi. — Papillomata arising from the mucous membrane some- times form very well-developed villosities in the pyloric region. In their interior one finds a very fine fibrillous network, formed by the prolongations of branched cells ; their surface is covered with cylindrical epithelium. Polypi may develop from myomata, lipomata, fibromata, and papillomata. They vary in size from that of a pea to that of a wal- nut. They may be pedunculated or attached by broad bases. The term polypus is only descriptive, and not so important, anatomic- ally, as the terms for other gastric neoplasms. In the structure of polypi at times the connective tissue, at others, the glandular ele- ment, predominates. They might, therefore, be classed logically among the fibromata and adenomata. They may present smooth, warty, or villous surfaces, the latter resembling the surface of a raspberry or at times of cauliflower. Villous growths presenting warty surfaces and a papillomatous structure are classed among the fibromata. They are covered by a single layer of cylindrical cells. Mucous Polypi. — Cornil (“ Gaz. des Hopitaux,” 1864, No. 20) has brought to light two cases of mucous polypi which had not manifested any symptoms during life. In one of these cases the red, mammillated, in places slate-colored, stomach, presented eight vegetations, from the size of a grain of wheat to that of a bean, which had their seat in the vicinity of the pylorus. These vegetations were soft, rosy, and injected with blood; their surface was irregularly mammillated, and they were formed exclusively at the expense of the mucous membrane. In the other case there existed only one pedunculated polypus, rounded like a cauliflower, and as large as a hazelnut. This tumor, formed at the expense of the mucous membrane and of the submucosa, was very vascular at 40 6o8 BENIGN TUMORS OF THE STOMACH. its center. Lambl (“ Beobachtungen aus dem Franz Joseph Kinder- spital,” Prag, i860, p. 376) has described a tumor as large as a pigeon’s egg, extending three centimeters along the fundus of the stomach, and covered by the mucous membrane, which had become thin ; no sign had revealed its existence during life. Debove found a mucous polypus by means of the tube, in a patient suffer- ing from nervous dyspepsia. Rokitansky attributed the formation of these tumors to chronic gastritis; they would thus develop around the glands of the papillae in unusual numbers and sizes. Wilson Fox also admits the part played by inflammation in the genesis of these polypi. Canus Govignon (“ Polypes de l’Estomac,” “These,” Paris, 1883) attrib- utes a certain influence to alcoholism. These polypi, whatever may be their structure, are somewhat rare. The first case was pointed out by Cruveilhier (“ Atlas de l’Anatomie,” xxx livraison, Fig. 2, p. 2) ; the stomach, the drawing of which he gives, con- tained ten pedunculate excrescences, one of which obliterated the pylorus. Andral (“ Clinique Medicale,” tome 11) in one case dis- covered laminated structures analogous to the gastric mucosa of ruminants. Ripault (1833), Mercier (1887), Castilhes (1843), Barth (1845), Richard (1846), Leudet (1847), Barth (1849), have reported a certain number of cases of the same character. Ebstein (“ Arch. p. Anat. u. Physiol.,” 1864) has collected all these observations, and has added 14 cases which he had himself obtained from 600 autopsies. Of the 24 cases thus collected, 1 5 occurred in men and 8 in women ; in 1 case the sex of the patient is not men- tioned. The frequency of these tumors increases after forty years ; in half the cases they are isolated ; in 1 case there were 50 of them, and in 2 cases there was a number varying from 150 to 200. Their form is variable — they are rounded, club-shaped, cylindrical, ramified; their color depends on their vascularization ; frequently they are pigmented. The mucous membrane which covers them is sometimes entirely smooth, sometimes villous, or thickened. They are usually located at the pylorus, and their size is in inverse ratio to their number. Lipoma (Murray, “ Fatty Tumor in Wall of the Stomach,” “Pathol. Tr.,” vol. xi, 1890). — The lipoma is also very rare. Starting from the submucosa, it sometimes makes a projection toward the gastric cavity, pushing back the mucous membrane which continues to cover it, but grows thinner in proportion as the tumor increases ; sometimes it pushes aside the muscular fibers MYOMA — LYMFHA DENOMA. 609 and succeeds in making a hernia under the serosa. A large tumor of this kind might cause digestive troubles by the dragging of its weight on the wall of the stomach, but the rareness of these cases interferes with an exact knowledge and description of their symp- toms. Orth has observed lipomata growing from the serosa in a pendulous manner (/. c. t S. 717). Myoma. — The myoma develops in the interior of the muscular layer, gradually projects under the mucous membrane, and occa- sionally ends by forming polypi — sometimes isolated, sometimes in numbers. These tumors do not differ in a histological point of view from those which may be found, for example, in the uterus, but their size rarely exceeds that of a pea or a cherry. Their development is not accompanied by any symptoms, and they are rarely discovered at the autopsy. (Myoma, see Virchow-Onkol, hi, 126.) Symptoms . — The symptomatology of these tumors is variable. Sometimes they become ulcerated, and Rondeau (“ Presse med. Beige.,” No. 18, 1881) has pointed out a case where their presence was revealed by serious hemorrhages; naturally, the observer was not able to diagnose the cause of this hematemesis. At other times, as in the case of Cruveilhier’s patient, the tumor may obstruct the pylorus and cause a dilation of the organ. Bernabes (“ Rivista Clinica di Bologna,” Juillet et Auot, 1882) had, in this way, the opportunity of observing a woman seventy years old who, for a long time, had vomited a few hours after meals, and experi- enced sharp epigastric pains, in the absence of characteristic symp- toms. At the autopsy there was found a polypus of six or eight centimeters, implanted on the anterior surface of the stomach, five centimeters from the pylorus. Five other smaller polypi were scattered on the pyloric antrum and along the greater curvature (Bruman, “ Th. de Paris,” 1883; Brissaud, “ Arch. Gen. de Med.,” 1885 \ Marfan, “ Th. de Paris,” 1887 ; Menetrier, “ Arch, de Phys.,” 15. Fevrier, 1888). Lymphadenoma. — The stomach may also be the seat of lym- phoid tumors. These likewise constitute a pathological rarity. Pitt (“ Pathol. Trans.,” vol. xi, 1890) has reported one case, and states that he has been unable to find more than seventeen in the literature on the subject. The patient had succumbed to phenom- ena which were all attributed to a tumor of the lungs, and to an empyema of the left pleura. Soft nodules were scattered over the stomach and intestines, which had perforated the mucous membrane, 6io BENIGN TUMORS OF THE STOMACH. or had made greater or lesser projections at its surface ; histologi- cally, all the characteristics of lymphadenoma were exhibited. The spleen, the mesenteric, and the bronchial ganglia were invaded; the liver and the kidneys were not affected, however. The neo- plasm develops in the mucosa and submucosa, and forms tumors projecting into the cavity. On the other hand, at times the serosa is first attacked. The muscular stratum then becomes more or less affected by distention, and a dilation of the organ becomes evident. In other cases the tumors which project into the gastric cavity become ulcerated, and the patient succumbs to a hematemesis, as in Reimer’s observation (“ Deut. Arch. f. klin. Med.,” Bd. xxxm, S. 632, 1879). To these phenomena are always added a diarrhea of varying seriousness; but when the tumors remain limited to the stomach, health may be little affected by it. Anatomically, one finds around the base of the tumor a hardening of the mucous membrane; the glands affected are in fatty degen- eration, while at their periphery there exists a characteristic reticu- lated tissue. The degenerated glands finally disappear, and there remains nothing more than the reticulated tissue of the tumor. Pedunculated adenomata, attaining the size of an apple, have been observed, which were composed exclusively of tortuous, irreg- ularly dilated gland tubules. Tumors may occur in the stomach as well as in the intestines, which anatomically and clinically must be considered cancers, and, having a pronounced glandular structure are designated as destructive or malignant adenomata or adenocar- cinomata. The case reported by Pitt (/. cl) is suggestive of this type. They have been considered under the malignant tumors. Cysts. — Retention cysts of the gastric glands occur in “ gastritis polyposa” and polypoid hypertrophy. Ruysch (“Adversaria Ana,” tome in, p. 1, Dec., 1732) described a gastric dermoid cyst contain- ing hair. Engel- Reimers (“ Deut. Arch. f. klin. Med.,” xxm, p. 632, 1879) describe a multilocular lymphangioma occurring in the outer gastric wall beneath a chronic ulcer of the lesser curvature. This cyst contained a milky liquid, produced by stasis of lymph in con- sequence of occlusion through inflammatory processes in the vicinity of the ulcer. Albers (“ Erlauterungen,” iv, p. 1 51) men- tions a cyst 2j{ inches long found on the lesser gastric curvature in a child. Foreign Bodies. — Foreign bodies are, in certain cases, capable of simulating a tumor, both by the subjective symptoms which they cause, and by the deception to which they give rise on palpation. FOREIGN BODIES IN THE STOMACH. 6 1 I A patient of Baillarger's (“ Union Med.,” No. 48, 1874) had kept in his gastric cavity for six years a zinc fork ; an epileptic, cited by Foville (“ Gaz. hebd. de Med. et de Chir.,” No. 18, 1874), had swal- lowed 28 dominoes; an ecclesiastical patient thus preserved his rosary in his stomach for a time. Labbe (“ De l’Acad. des Sci- ences,” 21 Avril, 1866) extracted a fork by gastrotomy. A sailor (“ Med. Chir. Transact.,” vol. xii, p. 72), cited by Ewald, in imita- tion of a juggler, swallowed 35 small knives, and succumbed only a long time afterward to digestive troubles. There were found at the autopsy 32 blades, more or less corroded: 30 in the stomach and 2 in the intestines. It is unlikely, however, that such objects as these could produce the signs of tumors. Schonborn (“ Berl. klin. Wochenschr.,” Nr. 17, 1883, und “Arch, f. klin. Chirurgie,” Bd. xxix, S. 609, 1883) has reported an observa- tion in which a gastrolith (movable tumor) was discovered in a girl fifteen years old, occupying the left half of the abdomen; it was easily pushed back under the left edge of the ribs, and very painful, both spontaneously and on palpation. The patient grew thin, would not tolerate any food, and her state became so serious that it was decided to perform a laparotomy, after having hesitated for a long time between the diagnosis of a movable kidney and that of movable spleen. The opening being made, the stomach was found distended ; it was cut into, and a mass of 281 gm. was found, formed by a net- work of short hairs, and molded to the form of the gastric cavity. The patient then confessed that four years before she had swallowed the hair in order to “ make her voice clear.” After this case, Schonborn made a careful collection of the known cases, and found seven of them, the oldest of which dates back to 1777. These cases include six women and one boy ; none were insane. All these subjects had died; some from peritonitis through perfora- tion, others from uncontrollable vomiting. One case ended in hematemesis, and Russel (“ Med. Times and Gazette,” June 16, 1869), who published it, reports that the tumor weighed four pounds seven ounces, was twelve inches long, five inches broad, and four inches thick. Never before had there been digestive troubles, and it had been supposed that it was a tumor of the spleen. In the observation of Inmann (“ Med. Times and Gazette,” July 3, 1869) the mass of hair was equally large. Best (“ Brit. Med. Jour.,” Dec. 11, 1869) reported a case of a woman thirty years old who, for sixteen years, had complained of pains after 6 12 BENIGN TUMORS OF THE STOMACH. meals, and had frequent vomitings, occasionally streaked with blood. For six years the pain had been almost intolerable, and hindered the patient from giving herself to any occupation. At the epigastrium a movable tumor was discovered, not sensitive to pres- sure, smooth, hard, extending from the right hypochondriac region to the left of the umbilicus, the prolonged palpation of which caused emesis. Peritonitis from perforation ended the case. The stomach and the esophagus were filled with a quantity of hairs, some of which were from ten to twelve inches long, and which altogether weighed thirty ounces. The patient had acquired the habit of swallowing her hair fifteen years before. Since Schonborn’s notice, Kooyker (“ Zeitschrift f. klin. Med.,” xiv, S. 203, 1888, also “ Weekbl. v. d. Nederl. Tydsch. v. Geneerk.,” December, 1887) has reported the case of an individual of fifty-two years old who, after having presented phenomena of cachexia, with hematemesis, suc- cumbed at the end of three years of sickness. During life a tumor the size of a small apple had been felt at the epigastrium ; and dis- placement of the spleen, a floating kidney, a cancer of the stomach, and a cancer of the colon were suspected, one after the other. On opening the stomach at the autopsy a renal-shaped foreign body was found, 18 by 8 cm., weighing 885 gm. ; two other masses were also discovered, the size of a hen’s egg. On examination with the microscope, these bodies showed some grains of starchy mat- ter and some vegetable cells, some of which contained chlorophyl, but no trace of animal substances. This case is analogous to that of Capelle’s (“Jour, de Med. de Bruxelles,” Fevr., 1861), who treated a woman forty-three years old for a tumor of the stomach, who had been ill for a long time. The symptoms were emesis, intense gastric pains, and constipation. The tongue was coated, palpitations frequent, the pulse small and w r eak. Under the xyphoid cartilage was found a hard, immovable tumor as large as a pigeon’s egg, which disappeared when vomitings, more violent than others, had caused the expulsion of a foreign body of nine cubic centime- ters, half softened, and formed exclusively of vegetable debris. The patient recovered. Lastly, Bollinger (“ Munchener med. Wochenschr.,” Nr. 22, 1891) published the case of a girl sixteen years old in whom there existed a hairy tumor which caused death by inanition. A malignant tumor had been suspected, and there was found in the stomach and in the dilated duodenum a tumor 55 cm. long by 11 cm. broad, and 28 cm. in circumference, formed by 500 gm. of hairs, which measured about 10 cm. HYPERTROPHIC STENOSIS OF THE PYLORUS. 6 1 3 The presence of foreign bodies in the stomach may give rise to the following signs and symptoms : The organ dilates, becomes displaced (Russel) ; the mucous membrane atrophies ; the pylorus may become expanded through muscular efforts to pass out the foreign body, which will act as a ball valve when expulsion is impossible; the peptic secretions disappear; the erosions allow the escape of blood in more or less abundance, and the patients usually succumb to a cachexia, since in the end alimentation becomes impossible. Therapeutic measures are useless in these cases. An explora- tory laparotomy is the only rational procedure. Erlach removed a myoma from the stomach weighing 5400 gm. (“ Centralbl. f. allge. Patholog.,” Bd. vi, 1895, S. 240). In the same journal (vol. vi, S. 717) Hansemann is reported as having found four peculiar tumors in the stomach : (1) A myoma with cystic degeneration ; (2) a sarcoma with hyaline degeneration and containing large calcareous bodies ; (3) a tumor of myxomatous nature ; (4) a tumor composed of finely fibered connective tissue, inclosing hollow spaces which contained cells in a state of fatty degeneration, simulating the cortical substance of the adrenal bodies. Professor Julius Schreiber reported a case of phyto- bezoar composed of the fibrous roots of a plant (“ Schwarzwurzel ”), which is a popular remedy for all sorts of ailments in Germany. The patient was a female peasant forty-five years old. The tumor very much resembled a floating spleen or malignant neoplasm. The diagnosis was correctly made and the woman successfully operated upon by von Eiselberg (“ Mittheil. a. d. Grenzgebieten d. Medicin u. d. Chirurg.,” Bd. 1, 1896, S. 729). In the “Jour, of the American Medical Assoc.,” March 5, 1898, A. H. Meisenbach ably reviews the literature on gastrotomy for removal of foreign bodies in the stomach. HYPERTROPHIC STENOSIS OF THE PYLORUS. Sienosing gastritis , hypertrophic stenosis of the pylorus , is a thicken- ing of the tissue about the pyloric region, caused by certain forms of chronic gastritis. The consequences of this obstruction and constriction may be and generally are as serious as if the pylorus was stenosed by malignant neoplasm ; except that in the former case the obstruction may be radically removed by operation, which 6 14 HYPERTROPHIC STENOSIS OF THE PYLORUS. is doubtful in cases of carcinoma or sarcoma. The condition was known to Cruveilhier and Andrae. In England the disease has been described by Brinton, Bennett, Habershon, Handheld Jones, and Hughes; and in this country by Einhorn, W. H. Welch, and the author. In the literature of the subject thus far presented one can dis- tinguish three similar types of this affection : In the first place, (i) gastric cirrhosis, the “ linitis plastica ” of Brinton. In this dis- ease the normal tissue of the gastric walls is replaced by prolifer- ated fibrillar connective tissue, which causes a marked reduction in the size of the organ. (2) The sclerosing gastritis of the French authors, first described by Hanot and Gombault in 1882, and later by Dubujadoux and von Kahlden. This disease ( gastrile chronique avec sclerose sous muqueuse hypertrophique') is characterized by changes in the other viscera, particularly in the liver, pancreas, kidneys, and especially in the omentum. (3) Congenital hyper- trophic pyloric stenosis. Two cases belonging to this class were reported to the Association of American Physicians in May, 1898, by Adler and Meltzer. This third type has no direct bearing upon the etiology of the benign stenosis of adults. We are concerned here only with types (1) and (2). The symptomatology of the sclerosing gastritis of Hanot and Gombault and of the gastric cirrhosis of Brinton is quite obscure, and it is probable that it is hardly ever diagnosed with certainty. In 1893 Tilger gave a his- torical review of our knowledge of stenosing pyloric hypertrophy (“ Virchow’s Archiv,” Bd. cxxxn, S. 290). A very exact and scientific presentation of the subject from the clinical as well as from the pathological standpoint has been given by Lebert (/. cl), who gives an account of six personal observations with the results of the autopsies. Einhorn reported four cases in January, 1895 (“ N. Y. Medical Record”), which recovered after operation ; and six other cases in which either surgical interference was refused or the patient temporarily im- proved by other methods, but the diagnosis of benign stenosis appeared to him quite certain. Personally, I have observed a benign hypertrophy of the pylorus in four patients. The fol- lowing is a typical case : A white laborer had suffered from motor insufficiency, absence of HC 1 and ferments, and presence of lactic acid for three years. I was on three occasions able to demonstrate a stenosis at the pylorus by my method of duodenal intubation. Operation was strongly advised, but as it TYPICAL CLINICAL HISTORY. 615 was repeatedly refused, an attempt was made to dilate the pylorus by means of larger and larger sounds introduced according to my system. The patient was unable to remain under hospital treat- ment continuously, and while the pyloric dilation by means of sounds rendered the pylorus sufficiently permeable, it inevitably contracted again within eight to ten weeks after cessation of treat- ment. The patient finally succumbed to his disease, and at the autopsy I found that the wall of the pylorus measured in the fresh state 2.3 cm. in thickness. All of the layers of the pyloric structure were thickened, but the true muscularis and the muscularis mucosae showed the greatest increase. Next in thickness was the sub- mucosa, while the peritoneal layer was only slightly thickened. The true mucosa had disappeared entirely from the pyloric region. In cutting a piece one millimeter in thickness into serial sections, I could not discover even remnants of gastric glands. In Lebert’s case there was still some glandular layer left, which was being pressed upon by connective-tissue proliferation. The greatest amount of work in the expulsive efforts of the stomach falls to the pylorus and the antrum pylori immediately preceding it. This region is naturally prone to muscular hypertrophy. The special incentive cause in these cases is a proliferating gastritis resulting in a hyperplastic inflammation, expressing itself most intensely in the pyloric antrum and sphincter, because all of the layers of the stomach except the glandular layer are most abundantly devel- oped in this neighborhood. Boas very aptly calls the catarrhal inflammation resulting in this condition a stenosing gastritis, to which designation no objection can be found because hypertrophy of the pylorus may occur under a variety of circumstances — for instance, corrosive agents may traumatically injure the pylorus, and the hypertrophic process may also arise from an ulcer. Pathologically, it is a chronic hypertrophic gastritis. Hirsch (/. c.) has reported a case of pyloric stenosis caused by a benign tumor that had originated from a peptic ulcer. Another fact justifying the nomenclature of Boas is that the symptomatology of chronic gastritis generally precedes the phenomena of this kind of stenosis for a long time. Boas reports three cases (“Archiv f. Verdauungskrankheiten,” Bd. iv, S. 47), but he is evidently mistaken when he asserts that neither Einhorn nor the author consider benign pyloric stenosis in our works, or that his three cases are the first of their kind that have ever been cured (/. c., p. 49). 6i6 HYPERTROPHIC STENOSIS OF THE PYLORUS. Before proceeding to a consideration of the diagnostic value of the prominent symptoms, a clinical history of a second case from our clinic will be in order. Mr. W. L., age thirty-eight, sick since February, 1892. Presents himself for treatment June, 1892. His suffering began with pressure, fullness, and disten- tion in the stomach. Bowels were at that time regular, and appetite was good. After the first six months of his suffering he had an interval of four months in which he was comparatively well, when a relapse of the symptoms of gastritis occurred, ascribed to the ingestion of crabs. In January of 1893 he consulted the author again, and was then suffering much from pain in the stomach after meals, and occasional attacks of vomiting following immediately after meals. An examination of the peristalsis of the stomach showed that at this time it was in a fairly good condition — no remnant of the meal of the previous evening could be found before breakfast the following morning. The contents of the stomach before breakfast consisted of from 20 to 50 c.c. of liquid containing much mucus, and showing presence of free HC 1 , but no food remnants. Results of chemical analysis (Salzer double test-meal) : Presence of traces of meat, egg, bread from the larger meal taken five hours before; no sarcinas, no Oppler-Boas bacilli; total acidity, 40; free HC 1 , 24; combined HC 1 , 12. For the pain and vomiting the patient was put on a milk diet, and small doses of codein. This was followed by prompt improvement, the patient returning to work. Six months later (July, 1893) the patient returned suffering from a repetition of the symptoms, which had returned intensified. The main suffer- ing was due to vomiting and pain. He was taught to use the stomach-tube himself, because now there were very evident signs of stagnation, as decom- posed remnants of previous meals were found every morning before breakfast. These remnants were the more abundant the more solid food the patient had taken, but if the diet had existed exclusively of milk and egg-albumen, or very finely scraped beef, no food remnants were found in the stomach the following morning. By my gastrograph it was found that the rate of peristalsis was now unmistakably impeded, though there was no evident dilation. The results of the analysis of the gastric contents were now as follows : Free HC 1 , 6; combined HC 1 , 4; lactic acid, a trace ; total acidity, 18 ; biuret reac- tion positive, erythrodextrin, o. The patient was allowed to take only a liquid diet. Nevertheless, 120 c.c. of offensive stomach-contents could be drawn away every morning before breakfast, which contained no free, but only combined, HC 1 , and lactic acid. Microscopically, large numbers of bacteria in threads were found, yeast in moderate amounts, no sarcinae, but many cylindrical and cuboidal epithelial cells. The urine contained no sugar nor albumin ; the amount in twenty-four hours was about one liter. Indican was present, but not in excess. Once daily the patient suffers from severe, cramp-like pains in the region of the stomach, but these attacks were not associated with vomiting. After the patient had mastered the technic of lavage he improved very much, and gained eighteen pounds in weight in eight months. In October, 1895, he returned again for medical treatment because he began to have vomiting attacks again, although he had been ex- ceedingly careful in his diet. He now had very aggravated motor insuffi- ciency, so that we once more attempted to dilate his pylorus by intubation. EXAMINATION OF THE ABDOMEN. 617 The lavage and liquid diet were continued. There were evidences of very severe chronic gastritis, as shown in a fragment of mucosa brought out during lavage by the patient. As HC 1 was absent on repeated examination, both in the free and combined form, the ferments were very much reduced. Rennin zymogen, active in dilution 1 : 30; discs of serum albumin placed in the filtrates, acidified with HC 1 , required four hours for digestion. Lactic acid present to such an amount as to give very distinct reaction with Uffelmann’s test. Examination of the Abdo 7 nen . — The stomach was so distended that its con- tours were very distinctly visible without artificial distention. No tumor could be palpated. Liver normal on percussion and palpation. Spleen and kidneys normal. Distention of the colon with C 0 2 showed it in normal position. By electrodiafhany the stomach was found to be not enlarged, though the lower curvature was distended to within one inch of the navel. By the use of liquid diet and daily lavage, together with intubation of the pylorus, the patient improved once more. As the diagnosis of the hypertrophic stenosis of the pylorus was now clear, the patient was once more urgently advised to undergo an operation. This he refused emphatically. After he left my supervision I did not see him again until June, 1896. He was so much emaciated that I failed to recognize him. He appeared like a patient in the last stages of pul- monary tuberculosis. The stomach was not very much dilated, but filled with putrescent material, and had descended lower than at the last examination. Notwithstanding artificial feeding with enemata, the patient died within ten days after this visit. At the autopsy I found the pylorus very much thickened — its walls in one place measuring three centimeters in thickness. The muscular layer showed the greatest increase in thickness. The mucous layer was lost entirely over this region. The thickening extended throughout the entire pyloric region of the stomach. The atrophy of the glandular layer extended all over the surface of the stomach. In the middle portion of the stomach, on the greater curva- ture, there was a small polypus about the size of a lentil. The passage through the pylorus was tortuous, so that not even a straight needle two millimeters in thickness could be made to pass. There were no histological evidences of car- cinoma. In plate X the histological features of chronic hyperplastic gastritis with pyloric stenosis are successfully reproduced. The enormous hyperplasia of the muscularis and the connective tissue, and the hypertrophy of the pylorus are especially clear. Age . — Pyloric hypertrophy in the sequence of hypertrophic gas- tritis is a disease occurring at a comparatively young age : thus the cases of Einhorn (/. c.), in which the ages are stated, show the following. Some of these cases were not due to stenosing gastritis but to other causes, probably cicatrices : Einhorn’s Cases. Number of Cases. Ages. Males, 4 28, 34, 40, 48 years. Females, 3 3 8 , 43, 5 8 “ Boas’ Cases. Number of Cases. Age. Males, 2 32, 47 years. Females, 1 43 “ 6i8 HYPERTROPHIC STENOSIS OF THE PYLORUS. Hemmeter’s Cases. Number of Cases. Age. Males, 2 23, 38 years. Females, 2 28, 36 “ Tilger (/. c.) reported 23 cases, as follows : 4 cases at the age of from 20 to 30 years. 7 “ “ “ “ 30 to 40 “ 6 “ “ “ ‘ ‘ 40 to 50 “ 2 “ “ “ “ 50 to 60 “ 2 “ f‘ “ “ 60 to 70 “ 2 cases over 70 years. If it were known how long these cases had been suffering before they came to the physician, a more uniform age could be arrived at. Thus, one of Einhorn’s cases suffered from digestive troubles for twenty years, another for eight, another for eighteen, another for fourteen. One of Boas’ cases had suffered for nineteen years, a second six, and a third two and a half years. In my own cases the one that came to me at the age of thirty-eight had been suffer- ing for four years ; and the female patient who consulted me at the age of thirty-six had suffered for three years. Deducting the time of the suffering already experienced from the age of the patient when presented for diagnosis, it is evident that a comparatively early period of life will be found to have been the stage at which these total 35 cases were first affected. From these figures another important moment in the diagnosis is evident — viz., the chronicity of the process. Symptomatology. — When the cases first present themselves, the first symptoms have existed for a long time. The anamnesis resembles the beginning of chronic gastritis. The complaints are fullness, pressure, distention, pain, eructation, and, occasionally, pyrosis. As the stenosing gastritis progresses, motor insufficiency of the first degree develops ; and then the principal symptoms are vomiting and pain. Gradually the classical signs of dilation of the stomach may develop ; but not in all cases where we have these symptoms is the stomach dilated. Owing to the obstruc- tion there are loss of weight, constipation, and reduction in the amount of urine. The appetite remains good, or it is, at least, good in the majority of cases for a long time. Size of the Stomach . — In the three cases we observed the size of the stomach was not markedly increased, and in the second male, aged twenty-three years, the stomach at the autopsy held only one ounce. This stomach in its actual size is represented in plate PLATE X, Hypertrophic Stenosis of the Pylorus from Chronic (Stenosing) Gastritis. Section through Thickened Pylorus and Normal Duodenum. The designations Fig. I and Fig. 2 denote the locations from which the histological drawings in the chapter on Chronic Gastritis were made. SYMPTOMATOLOGY OF STKNOSING GASTRITIS. 619 XI; in another case there was an undoubted gastroptosis. In only one of the cases, which Einhorn describes in detail, was the stomach dilated. In the other three it appears that this condition was not especially investigated. Boas describes dilation in but one of his three cases. Hematemesis has not been observed in connection with this disease by Boas, Lebert, Einhorn, or the author. If the hyperplasia has involved only the pylorus, a dila- tion is likely to result ; but if it has extended uniformly throughout the organ (linitis plastica), a cirrhotic contraction ensues. Tumor . — Einhorn found a palpable tumor in only one of his cases, and, similarly, Boas reports the existence of tumor in one out of his three cases. In the case described in this account, al- though the pyloric mass was as large as a hen’s egg at the autopsy, it had not been detected before death because the pylorus was in the normal position — under the right lobe of the liver. Condition of the Gastric Secretions . — The state of the secretion of the gastric juice will vary according to the duration of the disease and the period at which the patient presents himself. It is rational to presume that if the stenosis is brought on by a chronic gastri- tis, the longer the disease has existed the more atrophic will the mucosa have become and the less gastric juice will be secreted. Nevertheless, Einhorn found free HC 1 in one of his cases that had suffered for eight years prior to consulting him. In all, Einhorn gives an account of ten cases (“ New York Medical Record,” Jan- uary, 1895), but only four of them are described in detail; not all of these cases, it seems, were due to hyperplastic gastritis. They all showed retention of food, considerable quantities of gastric juice, presence of free HC 1 , absence of lactic acid, a high total acidity, and a long duration of sickness. Only in one of these cases did he find absence of free HC1 and presence of lactic acid. In the three cases reported by Boas free HC 1 was regularly absent, and in two cases, in addition to absence of free HC1, the ferments were very much reduced. All three had an unmistakable lactic acid reaction. In my cases free HC 1 was present at the begin- ning, but as the disease progressed, it gradually became less and less, and finally both free and combined HC1 was absent; then the reaction for lactic acid became positive. Boas considers the absence of free HC 1 and ferments an impor- tant factor in the diagnosis of hypertrophic stenosis caused by gas- tritis. This was the condition in two of my cases. It is evident 620 HYPERTROPHIC STENOSIS OF THE PYLORUS. from the autopsy report of one of my cases that it was undoubt- edly due to stenosing gastritis; free HC1 was absent, but the fer- ments active at a time when the diagnosis of hypertrophic pyloric stenosis could be made beyond a doubt. Diagnosis. — At the time when the patient first presents himself, the differential diagnosis between benign stenosing gastritis and carcinoma presents difficulties; but if we can clearly ascertain a history of many years of suffering, with alternating improvements and aggravations of the symptoms, and the increase and decrease of body weight, the improvement on carefully selected liquid diet and aggravation on a solid diet, we should be justified in suspect- ing a slowly developing benign process. Rosenheim (/. c.) has reported a case of benign stenosis* in which the presence of a tumor was recognized, and the same gastric chemistry as in car- cinoma, with the same pernicious tendency. A differential diag- nosis between such a case as this and carcinoma seems impossible. It may become necessary to distinguish between stenosis caused by gastritis and that caused by cicatricial contraction of the pylorus resulting from a gastric ulcer, and also from the dilation and food retention from primary and atonic gastrectasia. In the stenosis resulting from gastritis there will have been no preceding gastric nor intestinal hemorrhages, which will in most cases have occurred in case there is a cicatrix from an ulcer. If the stenosis is due to gastritis, free HC1 will eventually be absent. The fact that Einhorn found free HC1 in so many of his cases makes it probable that the constriction of the pylorus was not due to sten- osing gastritis, but to some other cause — cicatrices, for instance. A histological examination of the pyloric tissue does not seem to have been made in his cases. From primary atonic dilation stenosing gastritis can be differentiated by the absence of the symptoms of gastritis in the former. Visible spasmodic peristalsis indicates stenosing gastritis. The previous history of the case with its peculiar variations will be extremely important. Marked and lasting improvements, with increment of weight, do not occur in carcinoma. The periods of improvements in this latter disease, if they occur at all, do not ’ * A similar case originally reported by Dr. W. S. Thayer is often quoted in text-books as having'shown the same gastric chemistry as carcinoma and yet proved to be a benign tumor. Dr. Thayer has informed me privately that the detection of lactic acid in this case was due to an error in the preparation of the patient’s stomach before the test-meal was drawn for analysis. CARDIAC PLATE XI. 4 > PROGNOSIS OF STENOSING GASTRITIS. 621 exceed one month. In benign hypertrophic stenosis the symp- toms of stagnation are more amenable to treatment than in car- cinoma. The disturbances of the motor function in the latter dis- ease increase progressively, and the quantity of food remnants retained and found in the stomach before breakfast becomes more and more from week to week, no matter upon what diet the patient is placed. In hypertrophic stenosis the symptoms of stagnation may disappear for years under the aid of a liquid diet and lavage. Only in the very last stages of the disease does the stagnation be- come absolute. Whenever there are glandular swellings, coffee- ground vomiting, ascites, or evidences of metastases, presence of Oppler-Boas bacilli in the stomach-contents, the case will have to be considered carcinoma. The tendency is toward early diagnosis and early operation in both conditions. From this standpoint, a possible error in differentiating the two conditions will not be a serious one. The presence or absence of tumor in the region of the pylorus is of no diagnostic value in the differentiation in benign stenosis and carcinoma. If a tumor is present, it may as readily be a benign hypertrophy as a cancer; and if it is absent, it does not exclude the diagnosis of either of these conditions. It is of greatest importance in such cases, when the diagnosis lies between these two conditions, to take the weight of the patient frequently and analyze the gastric contents repeatedly. In a case which we had examined since June, 1892, and who died in June, 1896, free HC 1 was present ten months before the fatal termination; but after that, an examination made eight months before the end, showed no free HC 1 and excess of lactic acid. Prognosis. — The disease is fatal unless an operation is under- taken in time. The remarkable variations in improvement and aggravation are apt to mislead the clinician into a favorable prog- nosis. In order to form an approximate idea of the gravity of the case, it is necessary to test the motor function. We give preference to Hemmeter’s method by means of the intragastric rubber bag, and a small water manometer; because after trying the other methods for testing the motility we have found that they failed to give accurate results. There are three means by which we may gage the state of the motor functions clinically: (1) The amount of stagnating stomach-contents gained by the expression method, without addition of water, from the fasting stomach ; (2) repeated consecutive weighings of the body ; (3) repeated and consecutive 622 HYPERTROPHIC STENOSIS OF THE PYLORUS. measurements of the urine passed in twenty-four hours. During the beginning stages of the process, and as the stenosis is not very much advanced, it will be possible to introduce the amount of calories necessary to maintain the nitrogen balance by giving a liquid diet, consisting of milk, soft-boiled eggs, and predigested foods. When the gastritis has advanced, there is no secretion of HC 1 and ferments, and therefore there can be no gastric digestion of the food whatever, and it is offered to the pylorus in a much coarser state than if the secretions were normal. Treatment. — This may be palliative or curative. The palliative treatment consists in avoiding everything that might increase the gastritis. Alcohol, tobacco, irritating condiments, and spices must be excluded. The diet had best consist of milk and soft-boiled or raw eggs ; the latter only as long as free HC 1 is present in the stomach. After the gastric stagnation has advanced, and offensive residues are found in the stomach every morning, lavage is the treatment indicated. It is best carried out with water acidulated with dilute HC 1 , or with water containing one teaspoonful of table salt to the quart. Rectal alimentation is indicated in advanced emaciation from absolute pyloric stenosis, whenever immediate operation is not feasible. Medicinal Treatment. — This, in our experience, is of little or no utility, though according to the chemical nature of the case HC1, pancreatin, and papain may be employed. Duodenal Intubation . — A method by which a tube can be passed through the stomach and pylorus into the duodenum is original with the author, and was first employed at his clinic (“Arch. f. Verdauungskr.,” Bd. n, S. 85). I have carried out this method in a case of hypertrophic stenosis, but it was followed by partial success only. Although I succeeded in dilating the stricture of the pylorus for a time, the disease that caused it could not be cured thereby, and sooner or later^the stenosis resumed its former degree. The only method to cure the patient is by operation. Operation . — Every influence should be brought to bear upon the patient to obtain the consent for an early operation. If the steno- sis is absolute, and food no longer passes the pylorus, the opera- tion should not be postponed a single day. The types of operation that are available are gastro-enterostomy and the pyloroplastic operation of von Heineke-Mikulicz. The so-called pyloroplastic operation or digital divulsion of Loreta does not compare favorably in its results to the operative methods just mentioned. LITERATURE ON HYPERTROPHIC STENOSIS OF PYLORUS. 623 Postoperative Treatment . — After the stenosis lias been cured, the still-existing gastritis will require further dietetic, mechanical, and medicinal treatment, according to the principles laid down in the section on Chronic Gastritis. LITERATURE ON THE HYPERTROPHIC STENOSIS OF THE PYLORUS. 1. Boas, I., “ Ueber hypertrophische Pylorusstenose,” etc., “ Archiv f. Ver- dauungskrankh.,” Bd. IV, S. 41. 2. Codivilla, “ Gazeta degli ospitali die Milano,” 1888. 3. Dubujadoux, “Sur une variete de cirrhose encore inedite accompagnant la gastrite chronique avec sclerose sous muqueuse hypertrophique,” “ Gaz. hebd.,” 1883. 4. Einhorn, “ New York Med. Jour.,” January, 1895 ; see also “ Diseases of the Stomach,” by same author. 5. Finkelstein, H., “ Ueber angeborene Pylorusstenose,” “ Jahrb. f. Kinder- heilkunde,” Bd. xliii, S. 1, 1896. 6. Gran, Chr., “ Bemerkungen iiber die Magenfunktionen u. die anatom- ischen Veranderungen bei angeborener Pylorusstenose,” ibid. 7. Hammerschlag, “Boas’ Archiv f. Verdauungskrankh.,” Bd. 11, S. 19. 8. Hanot et Gombault, “Archives de Physiologie normale et Pathologique,” Bd. ix, p. 412, 1882. 9. Hemmeter, John C., and Wm. R. Stokes, “ Hypertrophic Gastritis and Pyloric Stenosis ” ; Memorial Vol. in honor of 25th Anniversary of Doctorate of Prof. Wm. H. Welch, Johns Hopkins University (Feb., 1900). 10. Hirsch, “ Freie Vereinigung der Chirurgen,” 22. Juni, 1896. 11. Von Kahlden, “ Centralbl. f. klin. Med.,” 1887. 12. Lebert, “ Die Krankheiten des Magens,” Tubingen, 1878, S 525. 13. Nauwerck, “Deutsches Arch. f. klin. Med.,” 1878, Bd.xxi, S. 574. 14. Rosenheim, “ Berl. klin. Wochenschrift,” 1894, No. 39. 15. Schoch, Inaug. -Dissert., Zurich, 1857. 16. Thayer, W. S., “Johns Hopkins Hospital Report,” 1893, No. 31. 17. Tilger, “Ueber die stenosierende Pylorushypertrophie,” “Virchow’s Arch.,” Bd. cxxxit, H. 2, S. 290. 624 MOTOR INSUFFICIENCY. CHAPTER VII. MOTOR INSUFFICIENCY. Gastric Atony or Myasthenia. — Gastrectasis ( Dilation oy the Stomach). — Obstruction of the Orifices. There is no uniformity in the classification of the various forms and degrees of abnormal enlargement of the stomach. The defective function in these cases is not commensurate with the size and capacity, but with the tonicity of the peristalsis. A very large stomach (megalogastria) may have a perfect motor function, and a very small stomach may have a defective motility. Boas recognizes a mechanical insufficiency of the first degree , which is a myasthenia or atony of the gastric muscularis in which the ingesta remain in the stomach too long, but finally are completely moved out into the intestines. There is no absolute retention of food, but simply a delay in the expulsion. Boas calls the fully developed dilation mechanical insufficiency of the second degree. Riegel differentiates : 1. Simple atony , or insufficiency of the stomach. 2 . Atonic or typical ectasia , or dilation. 3. Secondary ectasia , or pyloric stenosis with ectasia [dilation). Naunyn speaks simply of motor insufficiency, and Rosenbach of mechanical gastric insufficiency. Schreiber (Boas, “ Archiv f. Verdauungskrankheiten,” Bd. 11, S. 423), in attempting to select a designation which should signify the most constantly present con- dition of all these morbid states of motility, and one which should unite them all around itself, reached and suggested the term stasis stomach (“ Stauungsmagen ”),with permanent digestion or “perma- nently digesting stomach.” Besides being a cumbersome circumlo- cution, 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 atony — conditions which we are convinced really do exist — there is certainly no permanent digestion. Permanent digestion goes on in fully developed dilations with impaired peristalsis as long as hydrochloric acid and ferments are CLASSIFICATION OF MOTOR INSUFFICIENCY. 625 secreted. But as there undoubtedly are long-standing dilations with achylia gastrica, or loss of secretion (Einhorn), there can be no digestion in them. The fact that the food is overretained in them does not imply that it is digested; only in dilations that show hydrochloric acid and ferments can we speak of permanent digestion. The efforts of Schreiber to establish Reichmann’s chronic secretion as a complication of dilation with retained food products and permanent secretion caused by stimulation of the retained food, are very convincing. We shall speak of the pathogenesis of gastrosuccorrhea, or Reichmann’s disease, under the Nervous 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 classification as any is one based on Riegel and Boas, as follows : 1. Simple gastric atony or motor insufficiency or myasthenia without dilation. 2. Atonic dilation (motor insufficiency due to relaxation of the gastric walls) without pyloric stenosis. 3. Secondary dilation (motor insufficiency due to pyloric stenosis). The one common sign is not the retention of food nor per- manent 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 impassable obstacle, the fibers exhaust themselves in contending with an excessive resistance, and the dilation may then be considered as following on existence of the obstacle. In the first case the etiology is variable, and arises, finally, from a defect in the nutrition of the muscular layer or in the innervation ; in the other case it is purely mechanical. DILATION CAUSED BY A MECHANICAL OBSTACLE. Intrinsic causes of opposition to the passage of stomach-contents into the intestines, and of such a resistance to the contractions of the stomach that it dilates, are, first of all, the constrictions of the pylorus. These are generally the result of anatomical alterations 626 MOTOR INSUFFICIENCY. — viz., cancer, cicatrices, circular ulcer, or muscular hypertrophy of the pyloric sphincter. Nauwerk (/. c.) was one of the first to draw attention to hy- perplasia and hypertrophy of the pyloric sphincter as a cause of dilatation (which has been considered in a special chapter). A spasm of the pylorus, which can be compared to a spasm of the sphincter of the anus, can constitute an obstruction equally well. This spasm, which has been admitted by authors for a long time, — for reasons a little theoretical perhaps, — has been demonstrated since gastric surgery has permitted a more direct exploration. Martin (/. c .) has reported a case in which a pylorus large enough to admit the passage of two fingers brought on a considerable dilation by its spasmodic constriction, consequent upon a circular ulcer accompanied by considerable hyperacidity. Landerer (/. c.) is said to have proved the existence of a congenital pyloric constriction analogous to the congenital mitral constriction de- scribed by some authors. He collected ten such observations, and claimed that this orifice, though large enough during infancy, might undergo an arrest of development and remain very small, while the stomach grows larger with age ; a serious dilation would result from these diverging effects. (See Congenital Stenosis of Pylorus.) However, the obstacle does not necessarily have its seat in the tissue of the pylorus itself. In the chapter on Benign Tumors we have described the possibility of a polypus growing from the mucosa some distance from the pylorus and by means of a long pedicle capable of bringing about a dilation by becoming fixed, more or less, in the intestinal orifice, and thus causing its occlu- sion, acting like a ball-valve. Deiters (/. c.) has collected* a large number of observations, in which congenital malformations, abnormal foldings, diverticula, and atresia had provoked dilations by constricting the intestine in the immediate vicinity of the pylorus. An anatomical lesion of the duodenum — the cicatrix of an ulcer, for example — would produce the same effects by diminishing the caliber of the passage. The causes of extrinsic origin which have been observed to effect compression of the pylorus or duodenum are very numerous. Among these are peritoneal adhesions, circumscribed or not, the results of former inflammations. Fibrous bands issuing from a gastric cicatrix may so distort the normal location of the pylorus From the Anatomical Pathological Institute of Greifswald. ETIOLOGY OF DILATIONS. 627 (although not situated in the pylorus itself) as to compel the duo- denum to describe an abnormal course. Inflammations originating in the liver and the pancreas may be the starting-point of similar anatomical modifications. The head of the pancreas, so intimately connected with the duodenum, may become cystic or cancerous, and cause a duodenal stenosis by compression, with following dilation of the stomach. A con- genital displacement of the duodenum would bring about the same disorders (Cechini). Biliary concretions, by dilating the diverticu- lum of Vater, or by compressing the intestinal wall, may pro- duce a compression of the duodenum sufficient to bring about gastric dilation ; Grundzach has recently reported a case of this kind. Landau (/. c.), Bartels (/. c.), Warnek (/. c.), Mueller (/. c.), Litten (/. c.) } and other authors have studied the relations of dislocation of the right kidney to gastric dilation. Similar studies have been made in an interesting work by Bruhl, and Mathieu has also recently reported new cases (Societe Medicale d’Hopitaux). Patients presenting this coincidence of movable kidney and dilation of the stomach are usually young girls or women of the working class, who are in the habit of fixing their skirts above their hips, or lacing tightly, causing an external con- striction, which is shown by the presence of a permanent furrow. We append two illustrations showing the effect of tight lacing in producing distortions and dislocation of the stomach. Figure 39 illustrates the female skeleton and the funnel shape given to the lower thorax by lacing — the stomach being pressed down into approximately the position indicated by the dotted out- line, the antrum pylori coming immediately beneath the umbilicus. The stomach is not pressed upon directly, but is displaced by the pressure of the liver. This vertical position can also be brought about by the weight and dragging of neoplasms. A second malformation of the gastric cavity is the looped or tzvisted stomach , caused by lacing and probably by cicatricial con- tractions along the lesser curvature. The loop form is brought about by closer and closer approximation of cardia and pylorus (Plate XII). Dilation is easily developed from the vertical position, be- cause overretained ingesta dilate at first the antrum and later the entire gastric cavity. The vertical part of the duodenum, it must be remembered, is firmly adherent to the spinal column and can not descend ; if, therefore, the antrum or the pylorus lies lower, — as, for instance, in the loop form and vertical position, — the evacuation 628 MOTOR INSUFFICIENCY. is much more difficult than in the normal stomach position, because the ingesta must be lifted up to the pylorus. Only in the recumbent position and when the patient lies on the left side can the organ be evacuated. The musculature of such distorted and dislocated stom- achs is called upon to make excessive and superfluous expulsive efforts, whereby it readily becomes exhausted. The time of gastric Fig. 39. — Diagrammatic Illustration of the Mechanism Effecting Vertical Position of the Stomach. Compression of thorax by lacing, producing a funnel shape, forcing liver down upon the stomach. Antrum of pylorus (A) descends below umbilicus (U). digestion consequently becomes prolonged, and the gastric wall is overdistended and a motor insufficiency is gradually established. Kussmaul first called attention to kinking of the duodenum, occur- ring at the juncture of the movable horizontal and the fixed vertical portion of duodenum, and caused by the dragging of dilated or dis- torted stomachs. This constitutes an additional mechanical obstruc- tion, and has been observed by the author during a laparotomy — the PLATE XII. Malformation and Distortion of the Stomach Caused by Lacing or Tight Clothing, Belts, Etc. Figures I, 2, 3, and 4 illustrate the origin of the loop form of the stomach by approxi- mation of the cardia (C) and the pylorus (P). Figures 5, 6, and 7 illustrate the vertical position and descent of the pylorus (see text). LIBRARY OF THE UNIVERSITY ef ILLINOIS. DUODENAL ABNORMALITIES AND DILATION. 629 horizontal part of duodenum was kinked off and the first part fol- lowing the pylorus was dilated. H. W. Bettman has presented some instructive diagrammatic representations of the descent of the stomach and the formation of subpyloric (antral) pouch (“ Phila- delphia Monthly Medical Journal,” vol. i, p. 144). Men who wear a belt or strap may produce the same results. Lud. Knapp (“ Wanderniere bei Frauen,” Berlin, 1896) associates the frequency of floating kidney with abnormalities in the pelvic organs in women, causing constant dragging on the kidneys by means of the ureters. The right kidney may become displaced forward and inward, pressing upon the fixed, descending portion of the duodenum, which is situated between the hilum of the kidney and the vertebral column. Such partial obliteration of the intes- tine would bring about a slower and more difficult evacuation of the contents of the stomach ; but this is conceivable only if the dis- located kidney has become fixed in its abnormal position. We shall treat the effects of floating kidney more fully in the chapter on Enteroptosis. Ewald (/. c .) and Pertick (/. c.) have gathered together a cer- tain number of cases in which a hernia of the floating portion of the duodenum, or of the first part of the jejunum through a laceration in the mesentery, or a diverticulum of these portions of the intestine, has brought about an impediment to the normal course of the ingesta, and caused, in the end, a gastric dilation. ATONIC DILATION. Gastric atony is a condition of reduced or lost tonicity of the musculature. It is a state of sub- or hypotonicity, also very aptly designated as gastric myasthenia. (See special chapter on this subject.) Dilations resulting from this state that seem to be primary may be acute or chronic. The first kind, which are very rare, have for their cause either a traumatism or a surgical intervention (laparotomy), or else a serious infectious disease; Hilton Fagge (/. c.), Bartels (/. c.) f Montaya (/. c.) } and Lepoil (/. c.) have cited examples in which typhoid fever seems to have played the part of the chief cause. In this case the dilation seems to be 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 630 MOTOR INSUFFICIENCY. of food, an error committed so frequently by convalescents after they have been confined to one diet for a long time. Chronic forms of atonic dilations are dependent upon a great number of factors. Those addicted to excessive indulgence in food suffer first with distention of the stomach; then, later, with dila- tion. This phenomenon is comparatively frequent with persons into whose ordinary diet a large quantity of liquids enters; with excessive beer-drinkers, for instance, the beer acting not only mechanically by its volume, but also through the irritating and poisonous substances with which it may be adulterated. Debove (/. c.) has called attention to the drawbacks of prescribing milk in considerable quantities, and has cited, among others, a case of circular ulcer cured by the daily allowance of eight liters of milk; but an enormous dilation of the stomach resulted. In the chapter on Acute Gastritis we have pointed out that overfeeding produces a certain amount of gastritis. The dilation is produced under this double influence of the inflammation and of the disten- tion; without the addition of the first of these causes, megalo- gastria alone would occur. Simple chronic gastritis may result in a considerable atrophy of the muscular fibers of the stomach, which may lead to dilation of the stomach. The same may be said of hyperchylia, provided that it is one of the forms where a hyperacid secretion causes a pro- longed 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 retention in the stomach of undigested food, with fermentation thereof, when hydrochloric acid is absent. Drawn out by a weight more or less considerable, and distended by the gases that are developed in the putrefying mass, the mus- cular fibers gradually become diseased and lose their elasticity. The dilation found in consumptives, in chlorosis, etc., is due solely to chronic gastritis, which is caused by asthenia and the alterations in the blood, the results of these diseases. In diabetes both the chronic gastritis and superabundance of food cooperate in the alter- ation of the walls, and may finally lead to amyloid and colloid degenerations of the muscular fibers. Atony of purely nervous origin, concerning which the French writers Germain-See (/. c.) and Mathieu (/. c.) have published numerous researches, is held by them to be a consequence of “ crises,” by which term they mean successive and alternating NATURE AND CONCEPT OF DILATION. 63 I intervention of spasm and of atony of the gastro-intestinal tract. These crises are produced by an occasional and general cause, such as sad emotions, mental shock, neurasthenia, etc. The atonic form of dilation was first recognized, toward the end of the last century, by John Peter Frank (/. c.), who separates it distinctly from the forms caused by stenosis. The atony due to neurasthenia can be brought about by lesion of the central or peripheral nervous system, and the dilation will then depend on a deep-seated alteration either of the central organs or of the peripheral nerves. Bouveret, Dujardin-Beaumetz, and Glenard have represented general ptosis of the abdominal organs as the expression of a particular diathesis, a condition of relaxation of the tissues with unstriated muscular fibers ; and have suggested that there is a dilation depending upon this general state. The dila- tions resulting from nephroptosis are included in this class by Glenard, Debove, and Remond. (See Enteroptosis.) Pathological Anatomy. — Having already considered the patho- logical histology of the various causes of dilation, — viz., neoplasms, benign and malignant cicatrices, chronic interstitial gastritis, etc., — the pathological anatomy of the dilation per se is simple. At the autopsy of a subject dead from cancer of the pylorus, for instance, one finds the abdomen filled by a voluminous sac, which comes down more or less near the pubes. This sac, which repre- sents the stomach, having lost all its normal relations, and exces- sively dilated, may contain enormous quantities of liquid, and the ancient authors, who knew only the extreme cases, have cited ex- traordinary examples of this. (The history of the subject is given by Penzoldt, “ Die Magenerweiterung,” Erlangen, 1875.) Plem- pius (/. c.) is said to have seen a stomach that held nine pints of liquid; Stengel mentions a stomach containing 12 “measures”; Schurig, a stomach containing 48 liters; Henricus ab Herr found a stomach that filled the whole of the abdomen. Portal (quoted by Ewald and Pick) states that the stomach of the Duke of Chausnes, one of the greatest gourmands of his time, had a capacity of liters. The largest stomach observed by the author had a capacity of 4 liters, measured by his method. All the layers of the walls of the gastric sac have become thin ; and microscopically one finds atrophy of the mucosa ; at the same time the muscularis is now composed only of isolated bunches of muscular fibers, separated by the connective tissue. When the dilation is caused by an obstruction at the pylorus, hypertrophy of 632 MOTOR INSUFFICIENCY. the muscular wall is, as a rule, produced first; then interstitial sclerosis comes on, little by little, submerging the true elements, and the final atony of the wall is due to the disappearance of the contractile fibers. An apparent hypertrophy, through exagger- ated proliferation of the connective tissue, sometimes masks the actual atrophy of muscle-fibers in these cases which occasionally can not be distinguished from scirrhus, even microscopically. The muscular hypertrophy continues very long in the pyloric region, where it also attains its maximum point. The increased resistance and thickening of the walls sometimes results from ulcer, and may simulate a tumor. A dilated stomach may present variable forms due to the action of the special cause. If a cicatricial or scirrhous constriction causes the cardia and the pylorus to approach each other, the stomach will be pyriform ; but if the same lesion has plowed a trans- verse furrow, more or less deep, on the wall, a dilation in the shape of an hour-glass will be produced ; but the symptoms do not differ from those caused by occlusion of the pylorus. Symptomatology. — The tongue is, in most cases, coated by necrobiotic epithelium, mucus, and retained food debris, the breath frequently being very offensive ; there is generally a stomatitis, glossitis, or gingivitis present. State of the Appetite . — The appetite is normal at the beginning ; but when the disease has developed, it may be lost, or may become considerably decreased : 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 are no longer evacuated from the stomach into the intestine, diges- tion and absorption can not occur. In rare instances the patients may be tormented with hunger, and they are in a condition anal- ogous, so far as effects are concerned, to that of persons affected with an impassable stenosis of the esophagus. They try to satisfy their appetites, and, yielding to the solicitation of hunger, actu- ally present bulimic phenomena. In reality it is not hard to understand this difference, which depends practically on the nature of the obstruction to the course of the foods; anorexia is observed chiefly in cancerous patients and in those seized with chronic gastritis, while a cicatrix of a circular ulcer may have obliterated the pylorus without bringing about serious loss of appetite. Pyrosis . — The regurgitation of a certain quantity of very acid or SYMPTOMATOLOGY OF MOTOR INSUFFICIENCY. 633 alkaline ingesta often accompanies the eructations that pass through the cardia, causing intense pyrosis. Eructations and Gaseous Discharges . — In motor insufficiency of the first degree the gastric heaviness and the distention give way little by little, and if the patient takes his meals at regular intervals, his stomach at last empties itself and his p^tins disappear. But in motor insufficiency of the second degree generally the distress ceases only when more or less copious emesis has relieved the gastric cavity of the foods that 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 many different gases in considerable quantity. (See chapter on the Gases of the Stomach.) The principal gases are carbonic acid, hydrogen, oxygen, nitrogen, hydrogen-sulphid, and carbonic dioxid. Whenever there is stasis, presence of gases may be verified by directly extracting them from the stomach by the tube or by allowing the drawn gastric contents to stand in a closed vessel. This gaseous development is due to bacteria which may resist the antiseptic action of the hydrochloric acid, even when present in excess; some of these organisms have been isolated and cultivated. These fermentations, which are very frequent, are modified by salicylic acid or saccharin. Boric acid, carbolic acid, creasote, and chlorin water have no decided effect, in my experi- ence, except in doses that are incompatible with their thera- peutic uses. The great quantity of liquid contained in the stomach facilitates the development of anaerobic germs, giving rise to com- plex and toxic products of fermentation. Pain . — The pain of dilation is not marked ; the uncomfortable sensations are those of pressure, fullness, and distention. Naturally, if cancer or ulcer is coexistent with dilation, pain will be a prom- inent symptom. Vomiting . — In motor insufficiency of the second degree the at- tacks of emesis are quite characteristic. They are not so frequent as they are at certain stages of the development of cancer or of ulcer, and are generally separated from each other by variable but comparatively long periods, and they rarely occur at the time of the maximum of digestion. For one or two days a patient suffers, after each meal, from a sensation of growing uneasiness, and from a feeling of weight in the epigastrium, more and more painful; then, suddenly, often toward the middle of the night, he is seized 42 634 MOTOR INSUFFICIENCY. with very abundant vomitings, after which he can enjoy a little rest. The vomited material is sometimes composed of several liters of a mixture of solid food, drinks, and mucus. The quantity of vomited matter is a first-rate symptom of dilation, and allows it to be distinguished, for instance, from simple displacements of the stomach. Chronic gastritis, cancer, etc., may also give rise to slight hemorrhages, and in this case the very much modified blood remains a long while in the stomach ; the same phenomenon can be recognized in dilation. Boas has pointed out that the persistent presence of bile and of pancreatic fluid — of which the characteristics have been given — is an indication of stenosis of the duodenum, and is a valuable symptom of dilation resulting from the compression of this part of the intestine by a dilated gall-bladder or hepatic neoplasm, for instance. The vomited matter will have a more offensive odor the longer it has remained in the stomach. Later on in the disease, when the walls are distended, the vomiting comes on at greater intervals, the odor of substances vomited becomes more revolting, and then the emesis is rarely sufficient to evacuate the stomach ; the feeling of relief which at first followed is no longer experi- enced. Sometimes the vomitings cease after they have been very frequent — a grave sign of exhaustion. Symptoms of autointoxication from dilation have been described by Al. Pick (“ Wien. klin. Wochenschr.,” 1892, No. 46), Boas (/. c. p. 73), and J. Friedenwald (“ Med. News,” Dec. 23, 1893). A most exhaustive account of the autointoxication with motor insufficiency will be found in the works of Albu (l.c.) and Bouveret (/.£.). In dilation through an organic cause the disturbance of the general state will vary with this cause. Thus, it is observed that in cancerous patients the dilation is accompanied by the most evident cachexia. In ulcer, Reichmann’s disease, and chronic gas- tritis, dilation will be coincident with an emaciation more or less marked, but no cachexia. In the case of children, Comby and Moncorro have attributed to dilation caused by overfeeding a role in the etiology of rachitis. The latter author also considers it to be the cause of certain con- vulsions, of insomnia, of ringworms, of urticaria, and of bronchitis. Constipatioji . — Constipation is frequent and obstinate ; and not only are the stools rare, but the quantity of substances evacuated is also much less than in the normal state. This is a very valuable STATE OF URINE, BOWELS, ETC. 635 indication, for it shows the approximate amount of food that passes into the intestines. From four to six ounces of solid feces are normally discharged in twenty-four hours. In atonic dilation this amount is reduced to 2 y 2 ounces, and in extreme cases to 1 y 2 ounces, in twenty-four hours, on the average. The amount of water in the feces is normally 75 per cent. ; this is reduced to from 30 to 40 per cent, in dilation. The prognosis is influenced by the degree to which food may be made to take its normal course (Kussmaul). Persistent constipation or absence of stools indicates an incurable stenosis of the pylorus. Putrefactive diarrhea may alternate with constipation. Gastrorrhexis (Rupture of the Stomach). — Newmann (/. c.), Buist (/. c.) t Lautschner (/. c.), and Hoffmann have reported rupture of the stomach and sudden extravasation of its contents into the peritoneal cavity. Rupture may occur after a very sudden, acute dilation, or in the last stage of one of long standing. The tear generally occurs near an old cicatrix. A case reported by Chiari (/. c.) had a cica- trix near the lesser curvature, through which the tear occurred after overindulgence in food. In a case observed by Hoffmann (/. c.), in which a rupture of the lesser curvature had taken place, no other cause but food engorgement was assigned. State of the Urine. — The quantity passed in twenty-four hours may be reduced to 500 c.c. Boas makes use of the daily quantity for an approximate estimate of the degree of dilation. First degree. Quantity of urine in twenty-four hours, 1500 to 1000 gm. Second “ “ “ “ “ 1000 to 500 “ Third “ “ “ “ “ 500 gm. and less. The urine is generally alkaline ; the chlorids are diminished. The urine is frequently modified in quantity and in quality. The patients are in a 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 testifies ; thus the dilation brings about a deficient urinary secretion. Lastly, when the dilation accompanies an excessive secretion of hydro- chloric acid, and the latter is thrown out, either by frequent vomit- ings or by frequent lavage, the urine becomes alkaline. Nervous Phenomena . — Erb found increased galvanic and faradic irritability of all accessible motor nerves, with the exception of the facial. The increase of the galvanic irritability of the nerves is a more constant symptom than the increase of faradic irritability. 6 3 6 MOTOR INSUFFICIENCY. Von Frankl-Hochwart found the latter to be normal at times. Trousseau found that tetany could be caused by compression of the main nerve-trunks or compressing the principal blood-vessels of the limbs, so that the arterial and venous circulation was impeded. When this compression was kept up for two or three minutes, the tetany began, but would cease when the pressure was relieved. Chvostek discovered an increase of mechanical irritability of the nerves in the extremities, and also of the facial nerve in particular. This irritability became evident on tapping the nerves lightly with a percussion hammer or with the finger, which brought on rapid instantaneous twitchings in the muscles supplied by those nerves. On passing the finger over the face from the temporal regions down to the chin, distinct twitchings occurred in the muscles supplied by the facial nerve, because this stroke of the finger exerted an irrita- tion on ail branches of that nerve (Fr. Schultze). General State of Health . — -The general state of health is more deeply influenced by the cause of the dilation than by the dila- tion itself. Neurasthenia often causes an atony of the muscle- fibers of the stomach, the consequences of which can not but have a marked influence on the nutrition of the patient, encouraging and keeping up the neurasthenia. Diabetes, chlorosis, and great pyrexia, which may have caused the atony, provoke general dis- orders also, and it is difficult to distinguish from among the result- ing disturbances that which belongs properly to gastric atony. Cardiopulmonary Symptoms . — These have been considered in the chapter on the Influence of Gastric Diseases on Other Organs, in which I have dwelt on the effects of distention of the gastric cavity by gases hindering considerably the functions of the dia- phragm and disturbing the action of the respiratory and-circulatory apparatus. Dyspneic phenomena, or modifications in the sound of the heart and in the rhythm of the pulse, are frequently met with. Mattheides (/. cl) has gathered together a number of cases in which he observed a sensation analogous to that of globus hyster- icus in patients afflicted with dilation. He called attention to the fact that this sensation was aggravated when the stomach had sunk ; on the other hand, it diminished when it had risen ; from this he concluded that the displacement of the stomach so often accompanying the dilatation of this organ was the cause of this sensation of globus, through dragging on the esophagus. Schmidt (/. cl) is said to have verified, by a laparotomy, the existence of RESULT OF PERCUSSION AND PALPATION. 637 these anatomical disorders in a patient who had previously com- plained of the sensation of globus. The connection between the two is not at all satisfactorily proved, or even significant. Percussion, Palpation, and Auscultatory Percussion of the Stomach. — Osier (/. c.) emphasizes the fact that the diagnosis is often possible by inspection. Percussion and palpation allow us to ascertain the limits of the lower edge of the greater curvature, and, to a certain extent, to appreciate the degree of the ectasia. The percussion should be performed with the patient standing up, and again when lying on his back. The measured ingestion of a certain quantity of water will allow one to estimate the atony of the wall, and will at the same time furnish exact data on the displacement of the lower edge of the organ. The stomach may be distended by C 0 2 , and the colon by water, thus facili- tating the differentiation between the two. Other authors have proposed to perform the operation inversely, and to percuss the stomach made heavy by a certain quantity of water, while the colon is distended by gas (Ewald). Auscultatory percussion — i. e., percussing over the abdomen while a phonendoscope is simul- taneously moved over it and in constant connection with the ears — is of service in delineating the outlines of the stomach (A. L. Benedict). These precautions would make mistakes very diffi- cult ; they are available to general practitioners, which can not be said of the Rontgen rays and the electrodiaphane. Osier holds that when the distended stomach is outlined on the abdominal wall, one can usually follow its delineations with the eye, and, of course, much better by percussion. In the “ Philadelphia Medical Times” for May, 1891, Pepper reports a case of dilation caused by scirrhus of the pylorus in which there was a visible peristalsis. The gaseous distention has also the advantage that it allows the distinction to be made between true dilation and a simple dis- placement of the organ. By palpation the splashing sound can be investigated. This is easy to preceive when the stomach, the pylorus of which is con- stricted, is full of those liquid masses already mentioned in con- nection with the vomiting. But when the dilation is not very marked, the splashing becomes less clear, and Debove has recently shown that the intestines, when half distended by gases, are cap- able, under the influence of movements communicated by the fingers, of producing a sound so like that of the gastric splashing as to make the distinction very difficult. Chomel (/. c.) had already 638 MOTOR INSUFFICIENCY. drawn attention to this source of mistakes, and to that which de- pends on the presence of liquid and gas in the large intestine : “ The splashing in the stomach,” he says, “ might be con- founded with a similar sound of which the large intestine is some- times 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 in those who have been seized with serous diarrhea. The knowledge of these conditions and of the particular source of the gastric splashing sound is sufficient to distinguish it from in- testinal splashing. Jaworski (/. c .) has reported four cases of very audible splashing sound even when, on introducing the probe into the stomach, he had been unable to withdraw any liquid whatever. The author has observed this fact in a number of cases. It is not, there- fore, an unmistakable sign. For determining the location of the greater curvature, Thiebaut (/. c.), of Nancy, has devised an in- strument that 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 measure the vertical dimen- sion of the gastric cavity. This method impresses me as falla- cious. The methods of procedure based on the employment of salol, oil, iodid of potassium, etc., designed to determine the state of the motor functions and of the absorption of the mucous mem- brane, have been described. In dilation they give information of varying value, but inferior to that furnished by exploration with the sound. Dr. Harry Adler and myself have been able to map out the greater curvature with ease by means of a metallic spiral sound inclosed in a stomach-tube (Kuhn, Turck, Wegele). The {Eichhorst . ) Outline obtained by percussion. RESULTS OF TEST-MEAL ANALYSIS. 639 sound is readily palpable. I have already stated the signs by which one can recognize atony of a muscular wall : either pres- ence of debris of food in the morning before breakfast, or the prolonged retention of a test-meal in the gastric cavity. The Hemmeter gastrograph is a graphic method of obtaining motor records from the human stomach, and the results obtained there- with are generally reliable. (Plates in and iv, between pp. 72 and 73 -) Test-meals . — The gastric cavity should be washed out on the evening of the day before a test-meal is given. The substances extracted by this preliminary lavage are sometimes very abundant, and have the same composition as those vomited. They gener- ally become separated into three layers when allowed to stand : an upper one, frothy and turbid; a middle one, liquid ; and a lower one, composed of alimentary detritus of all kinds, or simply of amylaceous substances (hyperacidity). Organic ferments and sar- cinse will be discovered, and all the series of products that can, normally or abnormally, be contained in the stomach. If the motor insufficiency is caused by malignant neoplasm, the Oppler- Boas bacillus will, as a rule, be found in this material. In the morning before breakfast the gastric cavity, which has been cleansed the evening before, may again contain the normal products of se- cretion, or material which is rich in organic acids. The digestion of the test-meal will generally be 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 hydro- chloric acid will be found. When the normal HC 1 is absent, the filtered gastric contents will show excess of lactic and butyric acids. If the motor insufficiency is due to alcoholism, acetic acid will be a prominent constituent. Diagnosis. — Dilation or motor insufficiency of the second degree may have to be differentiated from atony, or myasthenia from gastroptosis and physiologically large stomach, or megalo- gastria. No sign, unless it is the presence in notable quantity of food in the stomach before breakfast, is pathognomonic. Bugge (/. c.) recommended the following operation : After determin- ing, by percussion, — the patient standing up, — the lower edge of the stomach, he drove the needle of a hypodermic syringe above the discovered limit. If the liquid extracted was acid, he concluded that the stomach had been reached. It is evident that this procedure is not without danger, and it is not even accurate. 640 MOTOR INSUFFICIENCY. I prefer the simple exploration by means of the sound, asso- ciated or not with artificial gaseous distention of the stomach ; these are the most available and practical methods for the gen- eral practitioner, and, in fact, suffice to distinguish a dilated from a displaced stomach, and from a naturally large stomach. But if they do not, the method of the author (p. 72) will leave no room for doubt. Gastroptosis (displacement of the stomach) will be fully consid- ered in a special chapter on that subject. The pylorus may be dis- placed, and may be freely movable below the epigastric region, without in reality causing any gastric disturbance. By palpation and percussion the greater curvature of the stomach can be made out below the umbilicus. One might then be very much disposed to suspect a dilation ; but on distention with C 0 2 gas, one sees not only the greater, but also the smaller, curvature outlined under the skin, and the outline of the whole stomach can be traced on the abdominal wall, and the limits of the corresponding resonant zone can be ascertained by percussion. The points of difference between a dilation and atony are the following: In the morning, before food has been ingested, the dilated stomach contains an accumulation of putrefactive products and food material, showing either excess of lactic and fatty acids or, when these are absent, abnormal amounts of HC 1 . In simple atony the stomach is, as a rule, entirely empty in the morning ; in atonic dilation it may contain trifling amounts of food, but not in a state of decomposition. In atony the bowel evacuations are less likely to be so few in number and so small in amount, and the total quantity of urine voided in twenty-four hours is normal or only slightly reduced. dilation the amount of urine is sub- normal, and it is concentrated and in rare cases contains diacetic acid and acetone. In megalogastria we are not dealing with a diseased stomach, and hence a differentiation is unnecessary. Tetany occurs only with dilation, but gastric vertigo is frequent in atony. The differ- entiation between a dislocated and a dilated stomach is facilitated by the clinical history. In a dislocated stomach the motor func- tion is frequently normal, and hence we find that emesis, if it occurs, does not bring out such very large amounts as in dilation. Diuresis and thirst are normal in gastroptosis ; in dilation thirst is intense, but on account of the regurgitation or vomiting of fluids, diuresis is subnormal. No matter where a stomach may be located PLATE XIII. Transillumination (electrodiaphany) of the stomach. The organ is filled with 600 c.c. of water, and has sunk downward to the left. The electric lamp has just reached the fundus ; on being pushed further, the intensest part of the transillumination would appear below the umbilicus. Gastrectasia. LIBRARY OF THE UNIVERSITY ef ILLINOIS. DIFFERENTIAL DIAGNOSIS. 64I within the abdomen, or how large it may be, it does not become abnormal until the motor function is interfered with. A Leube or Herschell test-meal or the Salzer double test-meal will instruct us concerning these points. The success of inspection, palpation, and percussion will depend upon the thickness and resistance of the external abdominal wall. When there is very little or no emaciation, 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 effer- vescent mixtures. But by means of the author’s stomach-shaped intragastric rubber bag, or by Einhorn’s electrodiaphane, it is possible to make the differential diagnosis without much difficulty. By the Hemmeter apparatus, which was originally designed to obtain records of the gastric peristalsis, it is also possible to measure the capacity of the stomach by determining the amount of air required to distend it within the stomach. (See p. 75.) This will at once enable one to diagnose a dilated stomach from one that has pro- lapsed but has retained its normal capacity. Einhorn’s diaphane is a practical method for demonstrating these two conditions to the eye. (See special article on Diaphany.) The Roentgen rays are also available for the same purpose, as demonstrated by the author. (Hemmeter, “ Photography of the Human Stomach by the Roent- gen Rays,” “ Boston Medical and Surgical Journal,” 1896.) Re- cently the author has used the following method : The dilated stom- ach is coated internally with bismuth subnitrate by means of the stomach powder-blower ; thereafter its outline can be distinctly recognized through the fluoroscope. The greater curvature may be outlined by photographing, by the Roentgen rays, a metallic spiral electrode that has been introduced and made to apply itself along the greater curvature, according to suggestions first made by Wegele. For private practice distention and the Einhorn electro- diaphane are most expedient, as they permit a diagnosis to be made by inspection. Debove and Remond (“ Maladies de l’Estomac,” p. 87) state that the execution of this method is difficult, and im- poses much suffering upon the patient. From what I have seen almost weekly with Einhorn’s apparatus, I differ emphatically from these observers, and believe a further experience with the apparatus will effect a change in their opinion. Diagnosis of the Cajise . — The cause is more difficult to detect than the dilatation itself. In this connection I refer to what has 642 MOTOR INSUFFICIENCY. been said in the consideration of ulcer, carcinoma, benign neo- plasms, etc., and their respective diagnoses. The anamnesis, the examination of the substances vomited, and the results furnished by test-meals will provide the principal data. The clinical history differs, in fact, considerably, according as one finds a dilation of cancerous origin or one caused by ulcer or gas- tritis. The effects of the ingestion of poisons have been con- sidered under Toxic Gastritis. The corrosive poisons frequently produce a cicatricial contraction of the pylorus. The significance of HC 1 in the gastric contents has been stated in the chapter on Car- cinoma. If the bile is always absent in the substances vomited, or in the gastric contents either before or after eating, one will be led to think of constriction of the pylorus ; this will probably be of cancerous origin if the hydrochloric acid is missing at the same time. The constant presence of bile and of pancreatic juice in the stomach would be a proof that the dilation is a consequence of a stenosis of the duodenum, which may result from a movable kid- ney, a fibrous adhesion, gall-stones, pancreatic, cystic, or hepatic neoplasm, etc. The author has devised a method by which a stenosis of the pylorus and of the duodenum can be accurately determined. (Hemmeter, “ Intubation des Duodenum,” “ Archiv f. Verdauungs- krankh.,” Bd. 11, S. 85. See also part first, this volume.) F. Kuhn, who belongs to Riegel’s school (Giessen), has also de- vised a method for sounding the pylorus, which is, however, a devel- opment of a revolving spiral sound first invented by F. B. Turck, of Chicago. The Turck-Kuhn method is very ingenious and simple ; but owing to the necessity of revolving of the spiral sound within the stomach, the method is not free from danger in cases in which we should suspect open ulcers or carcinoma, since the intragastric revolutions of the sound may bruise or tear the ulcer or neoplasm and set up hemorrhage or lead to perforation. The accuracy of these results, it is true, is not absolute ; but in practice, in associating them with other data furnished by the ele- ments of the diagnosis of each gastric affection, a diagnosis should, as a rule, be attainable. Prognosis. — The evolution of motor insufficiency varies accord- ing to the cause ; when it is a case of simple atony of recent date, a proper treatment — of which I shall speak again further on — may bring amelioration rapidly, and even cure. But when it is a PLATE XIV. Adhesions, Causing Motor Insufficiency but Retaining Stomach in Normal Position. S. Stomach. L. Liver. B. Gall-bladder. C , C, C. Colon. Adhesions of stomach to liver and gall-bladder (a 3 ) and transverse colon (a 4 ). Adhesions of hepatic flexure of colon to abdominal wall (a 1 , a 1 ). Adhesions of transverse colon to de- scending colon (a 5 , a 5 ) and of descending colon to abdominal wall (a 6 ). Adhesion of hepatic flexure to liver (a 2 ). The small intestine has been dissected away, only the mesentery remaining. The end of the ilium is visible in the lower left-hand corner. — ( From Author 1 s Clinic.') MALFORMATIONS OF THE GASTRIC CAVITY. 643 case of dilation with atrophy of the muscular coat, especially when there 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 gradually, unless one of the complications that have been mentioned appears and has- tens the end. Malformations of the Gastric Cavity. — For literature, see arti- cle by H. W. Bettman, “ The Shape and Position of the Stomach ” (“ Philadelphia Monthly Medical Journal,” vol. I, p. 1 2 1), contain- ing important anatomical contributions to this subject. As dila- tion is, in reality, a deformity of the stomach, a certain number of malformations and changes of form may be appropriately con- sidered in this connection. According to Debove and Remond, atresia of the gastric cavity results from diminution of work by the organ, through insufficiency of alimentary contributions. Inanition and constriction of the esophagus or of the cardia will thus have been the first cause of this atrophy. In other cases it is a cancerous infiltration, extend- ing over the whole wall, or a chronic gastritis 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 caliber of the stomach thus narrowed sometimes does not exceed that of the intestine. This condition has been referred to in the chapter on Hypertrophic Gastritis. When the upper diges- tive paths are open, attacks of emesis occur, appearing as soon as the quantity of food exceeds the very small volume of the stomach, the small caliber becoming still more evident when one comes to distending it with carbonic acid or to expanding it with the intra- gastric rubber bag. If stenosis of the esophagus or of the cardia exists, the passage of the tube becomes impossible, and the symp- toms of these constrictions assume enough importance to obscure entirely those which might be produced by the state of the stomach. The Hour-glass Stomach . — This type of deformed stomach may be : (i) Congenital ; (2) due to extensive cicatrization of a peptic ulcer ; (3) due to cancer, especially to scirrhus ; (4) due to an intense, spastic, and permanent contraction at the site of the preantral sphincter ; (5) due to peritoneal adhesions ; (6) due to abdominal tumors; (7) due to twisting of the stomach; (8) due to hernia of stomach through the mesocolon. Stoker (/. cl) has published one case in which the stomach was divided into two parts by a con- 644 MOTOR INSUFFICIENCY. genital furrow, and had never, during life, presented any functional disturbance. Iago (/. c) has related the story of a patient who succumbed when forty-two years old, after having suffered for ten months from uncontrollable vomitings; on the examination of the abdomen, a soft tumor was found underneath the liver which had been taken for a displaced right kidney; no tumor existed at the pylorus; emesis took place without pain, and was not preceded by regurgitation ; there was no cachexia. At the autopsy the stomach presented two dilated sacs, which communicated by a closed narrow passage, situated about the middle of the organ ; the index-finger could not pass this constriction. The cicatrices that had produced this deformity had been caused by a former disease, which appeared at the age of thirty and was character- ized by hematemesis and acute pains. A patient fifty years old, observed by Luigi Mazotti (/. c.) f experienced such intense pains after meals that she would squirm on her bed, and only found 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 toward the right side ; a narrow passage was situated between the two parts. The lower portion of the stomach had made a com- plete circle, and the contracted point was exactly the center around which this rotation had occurred. The upper part of the stomach was distended by gases; the lower part was empty and joined to the abdominal wall by adhesions. When the viscus had been replaced in its normal position, it was found that neither the ori- fices nor the wall presented any modification, and it was impossible to discover the cause of this displacement. Two cases of (i) Bour- get, (2) one of Schmid Monard, (3) one of Jaworski, (4) one of Bouveret, and (5) one of Watson Cheyne were diagnosed intra vitam. The most practical methods for such diagnosis are disten- tion with air or C 0 2 , gastrodiaphany, and the introduction of a sound, or, better, of the spiral sound of Kuhn or Wegele. The cases numbered 2, 4, and 5 were cured by operation ; the others improved under medical treatment. In another case, Chiari (/. c.) suspected a cancerous constriction of the pylorus in a patient who, in reality, had an intussusception of the stomach into the duode- num. Further particulars concerning similar cases can be found in the recent memoirs of Bettman (/. c.), Bauermeister (/. c.), and Saundby (/. c.), and in the theses of Kern (Inaug.-Dissert., Berlin, 1881), TREATMENT OF MOTOR INSUFFICIENCY. 645 Chiari (“Wien. med. Wochenschr.,” No. 42, 1890), von Hacker, in his monograph (“ Magenoperationen,” etc., published by Brau- muller, Vienna), gives a number of illustrations of stomachs divided into three parts by cicatrices or adhesions. (See Bibliography at end of this chapter.) Treatment of Motor Insufficiency of the First Degree ( Gas- tric Atony or Myasthenia). — Prophylaxis . — The muscu laris of the digestive organs may be weak by inheritance. Chlorosis, anemia, tuberculosis and cholelithiasis, exhausting hemorrhages, infectious diseases, typhoid, malaria, diphtheria, influenza, may bring on myas- thenia; and frequent and rapidly consecutive childbirths may, by causing increase of space in the abdominal cavity and loss of tone of the abdominal muscles, lead up to gastric atony. Insufficient mastication, hasty eating and deglutition, and defective teeth pre- dispose to atony. The treatment in all cases must seek the cause and adapt itself to its removal. Anemia must be treated by proper food, iron, extract of bone-marrow, and, in proper cases, arsenic. In women with gastroptosis and atony, the abdominal muscles must be strengthened and supported by proper bandages. The treat- ment proper includes diet, hydropathic and electrical procedures, massage, and medicines. Diet . — Patients with gastric atony may pursue one of two courses' with regard to diet : either they may eat frequently, but very little at a time, or they may limit themselves to two meals, — breakfast and dinner, — at 8 a. m. and 3 p. m. respectively, and permit the stomach to rest after dinner until the next morning. It can not be determined a priori which plan will give the best results, but for most cases the plan that secures most rest to the overworked organ is the most efficacious. Exclusive rectal feeding for three weeks has been followed by very good results. As water is not absorbed from the stomach, the quantity of liquids must not exceed from 1 to 1^ quarts in twenty-four hours, including all drinks, coffee, soups, etc. When there is a craving for more liquids than this, they should be introduced by enema. My experience with the frequent and persistent administration of milk, as observed in milk-cure sanatoriums in Germany, is dis- couraging. I believe this treatment to be a useless dietetic experiment in gastric atony, since the weight of the milk, used in such abundance, inevitably overdistends the organ. The special diet must be selected according to the state of the gastric secretions. If there is hyperacidity, a generous beef and 43 646 MOTOR INSUFFICIENCY. mutton diet, with limited carbohydrates, hard- and soft-boiled eggs, ham, tongue, oysters, duck, and deer in a finely divided form, is recommended ; of vegetables, carrots, spinach, soft-boiled turnips, beans, peas, and cauliflower, all finely cut up or as purees, are allowed. Potato, macaroni, rice, and farina gruel are permissible. If the hyperacidity is the cause of the atony, I favor restriction of proteid diet and a preponderance of amylaceous food, according to principles laid down elsewhere. Strictness should be observed concerning the use of alcohol, and when a trial proves that it injures digestion, I generally forbid claret, Rhine wine, and even beer. But when a trial with light wines demonstrates their bene- ficial action, about two ounces of wine with each meal may be permitted. Whenever the hydrochloric acid is diminished, the lighter meat varieties, — chicken, pigeon, birds, — fish, and boiled sweetbreads or calves’ brains, should be allowed only; but a larger amount of carbohydrates may be conceded. The special diet is stated more explicitly in the chapter on Dietetics. Constipation is a serious and a constant accompaniment of gastric atony; it must, therefore, receive our undivided atten- tion. Purgatives should be used only as a last resort, and the main reliance should be placed on diet, massage, and electricity. A pint of cold water, preferably Bedford magnesia spring- water, in the morning on an empty stomach, black (rye) or Graham bread, abundance of vegetables, — turnips, carrots, asparagus, tomatoes, rhubarb plant, beans, peas, lentils, — noodles, macaroni, barley, sweet compotes, plums, figs, apples, currants, cranberries, cider, buttermilk, kefyr, sour milk, honey. Figs, plums, and senna leaves stewed under constant stirring until intimately mixed, with sugar and lemon-juice added, is a useful laxative. When sweeten- ing is desired, milk-sugar should be preferred to cane-sugar. The use of these articles very rarely fails to bring about regular evacu- ations without medicines when massage and electricity are used in conjunction. Whenever drugs are positively unavoidable, I prefer cascara sagrada or aloes. In pronounced atony constipation can not be treated by this diet alone, because it increases the weight of the ingesta. The hydropathic treatment consists in cold morning sponge baths, cold wet packs, and Priessnitz bandages to epigastrium. In severe neurasthenic myasthenia I am in the habit of ordering a daily bath containing three per cent, of chlorid of sodium and two percent, of sodium bicarbonate; temperature of bath, 98° F. ; the TREATMENT OF MOTOR INSUFFICIENCY. 647 patient should remain in twenty minutes. When taken in the evening, this bath favors sleep. Electric Treatment. — Intragastric application with the Einhorn electrode within the stomach is most effective ; the faradic current is applied up and down over the spinal column and over the ab- dominal muscles. The constant current is applied in the same manner, in the strength of 20 milliamperes and for about ten min- utes. Systematic massage, both general and local, over the stom- ach is an important adjuvant. Medicinal. — This form of treatment should be as limited as pos- sible. The most approved tonic for the motor function is strychnin : R . Strychnin, sulphatis, 0.021 gm. gr. Elixir gentianse, 180.0 c.c. ^vj. M. SlG. — One tablespoonful three times daily. In anemia the gentian elixir with chlorid of iron may be substi- tuted. When the hydrochloric acid is deficient, it must be supplied ; when it is excessive, it must be neutralized by the following : R. Magnes. ust., 15.0 ^ss Bismuth carbonate, Natron, bicarbonat., aa 5 -° s;j -f- gr. xv Strychnin, sulphatis, o.i gr. iss. M. SlG. — One-half teaspoonful one hour after meals. Creasote and orexin are claimed by competent authorities (Pick and Penzoldt) to be able to excite the peristalsis ; the latter may be used when there is anacidity or subacidity. Creasote, in my ex- perience, does not increase gastric peristalsis. Lavage. — Asa rule, one will be able to get along without lavage in the first stage of motor insufficiency. But when the food re- mained in persistently overtime, I have seen improvement of mus- cular tonicity follow the rapidly alternating cold and warm intra- gastric douche. This exerts a powerful and stimulating effect also on the secretion, when it is defective ; when the latter is excessive, the douching should be carried out with alkaline water. Treatment of Motor Insufficiency of the Second Degree ( Fully Developed Dilation). — This may be considered under three headings: (1) Dietetic, (2) medicinal, (3) surgical. The diet is essentially based on the same principles as in simple myasthenia; the amount of liquid permissible must not exceed 1500 c.c. in twenty-four hours. With exaggerated vomiting and 648 MOTOR INSUFFICIENCY. pains, exclusive feeding by the rectum for fourteen days is recom- mended. A specified diet-list for both simple atony and pro- nounced dilation will be found on pages 235 to 237. It is impos- sible 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 weakness, 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 done with pure warm water, but the last washings are done with solutions adapted to the chemical and septic states prevalent in the organ. For instance, if there are great excess of hydrochloric acid or fermentation by sarcinae and yeast, sodium biborate or bicarbonate should be added, as these salts are not only antacid, but, with regard to these organisms, are also antiseptic. If there is butyric or lactic acid fermentation, boric acid (3 per cent.), salicylic acid (3 per cent.), or creolin or lysol (10 to 15 drops to a quart) should be used; but the stagnation can not be prevented from recurring by these means unless the motility is improved by other treatment. Electricity is indispensable : its method of employment, inter- nally and externally, has been described in a previous chapter. Massage undoubtedly improves the gastric musculature, but should be used only on days when the stomach has been washed out, because the mechanical compression may force stagnating masses into the intestines, thus spreading the putrefaction. Ab- dominal bandages properly adapted and applied have proved a val- uable palliative measure. Hy dr other apeutic applications are indis- pensable, and should be used as described in the paragraph devoted to the consideration of that treatment. Medicinal treatment has a twofold object: (1) To promote the motor function; (2) to prevent, as far as possible, gastric fermenta- tion 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 ^ of a grain for adults, t. i. d. Boas combines strychnin with an antifermentative in the follow- ing manner : B=. Strychnin, sulphatis, . 0.0022 gm. gr. Jg- Codein. phosphoric., 0.03 “ gr. | Bismuth, salicylici (basic), 0.5 “ gr. viiss. M. SiG. — One powder taken after each meal. TREATMENT OF MOTOR INSUFFICIENCY. 649 F. Kuhn has proposed salicylic acid (0.5 gm. to a dose), salicy- late of sodium (15 to 50 grains), or saccharin and sodium benzoate (of each, from 10 to 30 grains to a dose) to counteract gastric fer- mentation. Carbolic acid was first used by Naunyn for the same purpose. When there is marked lactic or butyric acid fermenta- tion, there is not a better agent than hydrochloric acid to coun- teract it: 20 to 30 drops of the dilute form in 2 ounces of water, through a glass tube, or in a large gelatin capsule of extra thick- ness (Aaron capsules). Among other remedies that are recom- mended are : Salol, naphthol, beta-naphthol, beta-naphthol bismuth, beta-naphthol benzoate, or benzonaphthol, hydrochloric and car- bolic acid. Bouchard is very enthusiastic concerning antifer- mentative treatment of gastrectasia, but it is certain that this treat- ment alone, without lavage and proper diet, is fallacious. Dujardin-Beaumetz employs : B. Bismuth, salicyl., Magnes. ustae, Sod. bicarb., . . . . aa 10.0 gm. gr. cl. M. SiG. — To be divided into 30 powders ; one powder after meals. Our formula for gastric fermentation, particularly when asso- ciated with putrid diarrhea, is : Beta-naphthol benzoatis, . . 8 3 b Bismuth, salicylatis, . . . . 8 3 b Magnesiae ustae, .... . 8 3 b Saccharin, - o -5 gr. viiss Menthol, gr. xvj. SiG. — To be divided either into 12, 24, or 36 powders, to suit the indications; if there is much fermentation, it should be divided into 12 powders, and one given three times daily. Otherwise it should be divided into 24 powders, and one given every three hours. Ewald’s formula for prevention of gastric fermentation is the following : B • Resorcin, resublim., . . 5.0 gr. lxxv Bismuth, salicyl., Pulv. rad. rhei, Natrii sulphur., . . aa 10.0 gr. cl, about 3 iiss Sacch. lact., 15.0 gr. ccxxv, about £iij + ^ ij- M. SiG. — Make a powder; one-half teaspoonful twice daily. When HC 1 secretion is lost, dilute HC 1 should be administered, according to the formula given on page 475 ; if HC 1 is not well tolerated, pancreatin should be tried, according to the principles given on page 344. 650 MOTOR INSUFFICIENCY. For improving the appetite, strychnin, orexin, HC 1 , and lavage are the most approved means of therapy. For vomiting, lavage is the most efficacious treatment; but if it fails, resorcin (2 grains in y 2 of an ounce of chloroform water), ora hypodermic injection of morphin (jr of a grain), and atropin sul- phate (‘2"o"0‘ of a g ra i n ), will be called for. Minute doses of calomel (tV a grain) every hour act as gastric sedatives in some cases. As a rule, menthol and chloroform do not disappoint when used for the relief of vomiting. The following formula is practical: R . Menthol, 1.0 gr. xvj Chloroform., 1. 5 gtt. xxiv Elixir simplic., q. s. 60.0 f^ij. M. SiG. — fgij every hour. Insomnia must sometimes be treated, as these patients impera- tively need rest ; for this purpose chloral, 1 5 grains by enema, is most advisable. Correction of hyperacidity will often induce sleep. Sulphonal and chloral combined, eight grains of each, will produce a more lasting sleep than if either is used alone. Trional is recom- mended for the same purpose by Boas. Surgical Treatment . — The operations that have been suggested for the relief of motor insufficiency vary according to the object to be accomplished. Motor insufficiency from simple atonic dila- tation may be relieved by reducing the size of the stomach by gastroplication or gastrorrhaphy (Weir).* If the pylorus is stenosed by a simple cicatrix or a hyperplastic sphincter, Loreta’s digital divulsion of the pylorus is an operation that, judging from the statistics, is an unsafe and unreliable pro- cedure. The pyloroplastic operation of von Heineke-Mikulicz, which Boas terms the ideal surgery for the relief of pyloric stenosis of a benign nature, produces more permanent results. Gastro-enterostomy and resection of the pylorus, as well as gastrorrhaphy, — an operation originated by Dr. Heinrich Bircher, a Swiss surgeon, — will come under consideration. The indications * In June, 1899, Dr. Randolph Winslow operated on a well-known Baltimore phy- sician who had an enormous gastrectasia and a kidney that could be moved about ad libitum on the right side. The doctor, although sixty-four years old, submitted to opera- tion by my advice. The stomach was reduced by four plaits extending from cardia to pyloric antrum, and, at the same time, a nephrorrhaphy executed. He made a perfect recovery, was doing well on December 16th, 1899, and, in his own words, was “just beginning to enjoy life.” DIETETIC AND SURGICAL TREATMENT. 65 I for these operations and their technic, are subjects concerning which the reader must be referred to the chapter on Gastric Sur- gery. The larger portion of dilatations are undoubtedly due to some obstacle to the exit of the chyme (ischochymia, 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 all found in the stomach itself, for in the account given under the etiology, dis- tended gall-bladder, gall-stones impacted in the diverticulum 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. DIET FOR MOTOR INSUFFICIENCY OF THE FIRST DEGREE — ATONY — MYASTHENIA. — {Boas.) Calories. 8 A. M. — 100 gm. of milk, 50 gm. of toast, 30 gm. of butter, 401.2 10 A. m. — 50 gm. of wheat bread, 30 gm. of butter, 60 gm. of scraped beef, 41 5.2 12 m. — 150 gm. of boiled beef, 50 gm. of potato puree or macaroni, . . 439.3 3 p. m. — 100 gm. of milk, 50 gm. of Zwieback, 401.2 7 p. m. — 100 gm. of cold ham or beef, 150 gm. of wheat bread, 30 gm. of butter, 557-5 Total, 2214.4 About three ounces of good port wine or claret may be allowed during the day. DIET FOR MOTOR INSUFFICIENCY OF THE SECOND DEGREE —PYLORIC STENOSIS— MYASTHENIC DILATION. — {Hemmeter . ) Calories. 8 A. m. — 100 gm. of Mosquera’s beef chocolate or Somatose chocolate, or 50 gm. of tea with 50 gm. of milk (sweetened with saccharin, no sugar), 50 gm. of toast, 195.5 10 A. m. — 100 gm. of scraped lean beef, 437-0 30 gm. of toast, 77.7 10 gm. of butter 71.3 Total, 586.0 12 m. — 150 gm. of roast beef, 320.7 50 gm. of potato puree, 63.7 Total, 384.4 In place of the potato puree, the same quantity of spinach, car- rots, peas, or beans may be allowed as above. 652 MOTOR INSUFFICIENCY. Diet for Motor Insufficiency of the Second Degree .—{Continued.) Calories. 2 p. m. — 50 gm. of cream, 107.30 4 p. m. — 100 gm. of tea or coffee^with milk (no sugar, but saccharin), 50 gm. of toast, I95-50 7 p. m. — 100 gm. of broiled fresh fish or oysters, 7 1 .7 5 50 gm. of wheat bread, 129.00 10 gm. of butter, 71.30 100 gm. of cream, 214.00 9 P. m. — 50 gm. of cream, 162.30 Total, 1885.15 In atony and dilation, as well as in carcinoma, experience is the best guide for enlarging and varying the diet. Every new article of diet must at first be tried with great caution ; if liquids are well tolerated, they may be increased, and soups may be 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 incidentally instruct the physician concerning the digestibility of new foods and, what is more important, the state of the motor function. OBSTRUCTION OF THE ORIFICES. Obstruction of the cardia and of the pylorus may be organic or functional. The former is, as a rule, caused by the consequences of carcinoma, peptic ulcer, phlegmonous or toxic gastritis. The functional obstructions are due to cardiospasm and pyloro- spasm. These conditions have all received proper consideration in other chapters. There are other very rare causes, which merit attention more from a pathological than from a clinical standpoint. Obstruction of the Cardia. In considering the organic causes which most frequently lead up to stenosis of the cardia, it will be important to compare the table that gives the situation in the stomach of 793 gastric ulcers (p. 497) with the table on page 545, giving the situation in the stomach of 1300 cases of carcinoma. Thus it will be found that the pylorus is affected in gastric ulcer in 12 per cent, of the cases, and the cardia in 6.3 per cent, of the cases, making the total per- centage of involvement of the orifices by gastric ulcer 18.3 per cent. In carcinoma the pylorus is affected in 60.8 per cent., and OBSTRUCTION OF THE ORIFICES. 653 the cardia in 8 per cent., of all the cases. The orifices being, therefore, involved by carcinoma in 68.8 per cent, of all the cases. The greater frequency of malignant neoplasm as a cause of sten- osis of the orifices is evident from these figures. The obstruction of the cardia may be classified under the following types : 1. Congenital Stenosis. — Like congenital stenosis of the pylorus, this is a rare disease, and may be partial or complete. If the sten- osis is absolute, the child will die very shortly after birth from in- anition. In partial congenital stenosis of the cardia it will be impossible for solid food to pass, but as the infant lives exclusively upon milk, the condition may exist fora long time without threat- ening life. I have seen one undoubted case of congenital stenosis of the cardia in a child six years old in which, after careful exami- nation of the esophagus and stomach, the symptoms of dysphagia could not be explained in any other way. This child has been permanently relieved by gradual dilatation of the cardiac ring. Two years have elapsed, and the child remains well. 2. Stenosis Due to Compression. — These are brought about by the pressure of disease or dislocated neighboring organs — for instance, aortic aneurysm, tuberculous or syphilitic mediastinal lymph- glands, neoplasm of the pleura and lungs, diverticulum of the esophagus. 3. Obturation stenosis , due to occlusion of the lumen by the most varied kind of foreign bodies — artificial teeth, coins, ingesta, masses of the thrush fungus ; by polypi which, arising from the wall of the pharynx or esophagus, may extend down into the lumen of the cardia; protrusion of a portion of the mucosa of the esophagus, as in phlegmonous esophagitis or abscess of the cardia or lower end of the esophagus. 4. Stenosis caused by cicatrices , resulting from gastric ulcer, phlegmonous or toxic gastritis, corrosive destruction of the cardia by acids or alkalies or other caustic materials, and in the healing of syphilitic neoplasms and ulcers. 5. Carcinomatous Strictures. — These compose from 90 to 95 per cent, of stenoses of the cardia. 6. Cardiospasm , causing spastic stenosis and cramp of the muscu- lature. Stenosis of the cardia by simple hypertrophy of the mus- cular layer is unknown. This condition occurs frequently enough in the neighborhood of the pylorus to merit its consideration in a special chapter. Stenosis of the cardia has been known to occur in the sequence of compression of the lower end of the esophagus, 654 MOTOR INSUFFICIENCY. caused by pericardial exudates, cardiac hypertrophy, curvature of the spine, aneurysm of the aorta. When the lower end of the esophagus is compressed only on one side by any one of the con- ditions enumerated, this tube may escape to one side and thereby avoid complete occlusion ; but when it is compressed from several or all sides, absolute stricture may result. When the cause of the trouble is in the immediate neighborhood of the foramen rotundum, through which the esophagus perforates the diaphragm, the symp- toms may be identical with those of stenosis of the cardia. Symptomatology. — This has been given under the heading of Carcinoma of the Cardia, page 566. Suffice it to say that the char- acteristic symptom is dysphagia. When the stenosis is due to carci- noma, the dysphagia may sometimes become temporarily alleviated. This is due to exulceration of the malignant tumor. At first only solid food becomes arrested in the lower portion of the esophagus, but later on not even liquid food will pass the constriction. The patients accurately locate the obstruction to swallowing at the level of the ensiform cartilage. In the beginning of the stenosis repeated swallowing will succeed in passing on the morsels of food through the constriction. Careful chewing and thorough insalivation facili- tate the act. Sometimes the sufferers seek relief by drinking water after the solid food or by stroking downward along the front of the throat and chest. If solid food clogs up the upper or middle third of the esophagus, the signs of dyspnea become very intense. In the beginning of the stenosis practice in swallowing seems to make the act easier. After each pause, when nothing has been swal- lowed for a long time, the act becomes more difficult. The food is regurgitated after varying periods. At first it occurs only during ingestion or shortly afterward, but later on a dilation develops above the constriction, and the food is retained longer. Then regurgitation occurs between meals. The food which is brought up is usually covered with mucus ; in carcinoma, with blood and mucus, and it is then in a state of putrefaction. The food is gen- erally neutral or slightly alkaline. Its chemical character gives no evidence of its having entered the stomach. Blood in the regurgitated food may come from carcinoma, ulcer, or cardio- esophageal veins in a state of passive congestion. For the physical signs of stenosis of the cardia see page 566. The condition of appetite and thirst is variable. Generally, the patients complain of great hunger and excessive thirst. Diagnosis. — The physical inspection of the abdomen is sugges- DIAGNOSIS OF STENOSIS OF THE CARDIA. 655 tive. As no food can pass the stenosis, the stomach and the intestine having been empty for a prolonged period, the abdominal walls are very much retracted and sunk in beneath the level of the costal arch. In attempting to locate the stenosis by introducing an esopha- geal sound, a very soft instrument should at first be used, in order to avoid injury to a possible esophageal or gastric ulcer or carcinoma. In the chapter on the Technics of the Stomach-tube we have re- ferred to a case from Penzoldt’s clinic, in which the stomach should have been washed out in the morning, but, for some reason, this was postponed until the evening. On the same afternoon the patient died of rupture of an aortic aneurysm into the esophagus. Stenosis of the cardia might possibly be due to an aortic aneurysm, and sounding of the esophagus may lead to rupture of the sac. The constriction is generally located by means of the tube as being about forty centimeters from the point where the incisor teeth touch the introduced sound. This is only an approximate figure, as the length of the esophagus will vary with the height of the person. In one case of carcinoma of the cardia in our experi- ence, the tube could be introduced for fifty centimeters before it struck the stenosis. (For rules to determine the length of the esophagus in any individual, see Hemmeter, “ New York Medical Journal,” December 28, 1895, quoted on p. 1 1 5 of this volume.) In case of carcinoma patient research will eventually result in the discovery of a fragment of the neoplasm which in these cases is generally found in the eye of the tube. Cardiospasm occurs mainly in neuropathic individuals. It differs from the organic stenosis of the cardia from the fact that the obstruction is not constant, but intermittent. Large sounds will pass as readily as small ones after a little practice in the introduction, and the stenosis will disappear entirely under anesthesia. Prognosis. — Though dependent on the fundamental alteration causing the stenosis, it is generally unfavorable, except in cardio- spasm. Prognosis is absolutely hopeless in carcinoma. When the stenosis is due to cicatricial contraction, the orifice may remain patent sufficient to carry on nutrition, and for a long time the narrowing process may appear stationary. Treatment. — The treatment is, in the main, the same as for carcinoma of the cardia (vide). Nutritive enemata are, in my ex- perience, best used as soon as the diagnosis of obstruction is certain, even if a limited amount of food can be introduced through the mouth. Stenosis due to cicatricial contraction can be succes- 656 MOTOR INSUFFICIENCY. fully treated by gradual dilation of the constriction by means of sounds of greater and greater thickness. Sometimes the cardiospasm is due to an ulcer that has been healing very slowly, or possibly to a small erosion due to the passing violence of some sharp body in the food. In one case of dysphagia, which was due to ulcer of the cardia, we relieved the pain and made swallowing possible by a kind of local treatment. A small sponge, saturated with a four per cent, solution of cocain, was placed in the end of a stomach-tube that had only a side opening, the lower end of the tube being bluntly closed ; when the lateral opening had reached the stenosis, the cocain solution was pressed out by a wire which terminated in a small round ball resting upon the sponge, and emptied the cocain on the painful surface. Patients with stenosis of the cardia fear starvation, and justly so. The moral effect of sufficient nutrition is a great one. I am in the habit of feeding all patients into whom a tube can be passed at least three times daily with food represent- ing a caloric value beyond what is really required. Benign strictures of the lower end of the esophagus and of the cardia have been cured by the patients themselves, after they had ac- quired the technic of sounding and dilation. The longer the sound remains in position after it has passed the stenosis, the more effective will be the widening process. Leyden has suc- cessively employed permanent cannulas, which remain in situ for several days. He has even employed them in carcinomatous con- strictions in the lower end of the esophagus. These cannulas can be introduced by the aid of the stomach-tube. They are from six to eight centimeters long, and are attached by means of strong cords to the ear or around the neck. The diet should consist of raw eggs, milk, thin chocolate, meat powder, somatose, gelatin ; also ice-cream and frozen custard may be allowed, but must be warmed in the mouth and eaten slowly. Egg-nog should not con- tain too much brandy. Not much should be expected from medici- nal treatment. Morphin or codein can not be avoided for the relief of pain. For the pain of cancer of the cardia we have found chloral hydrate (gr. xv, t. i. d.) especially effective. Iodid of potassium and sodium, methylene-blue, and arsenic have been recommended for cancerous stricture. Personally, I have no faith in these medications. The iodids should be tried, however, if there is a suggestion or evidence of syphilis about the case. When a dila- OBSTRUCTION OF THE PYLORUS. 657 tion of the esophagus has formed above the constriction, it is well to wash out the pouch every morning, as one would wash out a dilated stomach. This will prevent a septic esophagitis. The mouth, nose, and throat should be kept disinfected by antiseptic sprays and gargles. Gastrostomy will prolong life if performed early enough. In our experience even if the stenosis is due to a carcinoma, it will not progress so rapidly when it is kept free from food, and disin- fected daily by lavage from above. But when gastrostomy is un- dertaken in benign stenosis, it not only makes possible the proper feeding of the patient, but the stenosis can be dilated after the operation by intubation from the gastric end of the esophagus. Exploratory laparotomy may reveal the fact, unknown before the operation, that although the stenosis of the cardia was due to a carcinoma, this neoplasm was sufficiently below the diaphragm to be entirely removed. The recent success of Brigham and Schlatter after a total extirpation of the stomach makes it conceivable that large portions of the cardiac end and fundus can be removed, and the remainder of the healthy stomach or the jejunum attached to the stump of the esophagus. (See section on Surgical Treatment of Organic Diseases.) Obstruction of the Pylorus. Stenosis of the pylorus is, in the majority of cases, a consequence of organic disease. Idiopathically it occurs very rarely in chil- dren in the form of congenital atresia. Meltzer and Adler each reported one such case to the meeting of the Association of American Physicians in May, 1898. Maier has collected thirty-one cases of this kind (“ Virchow’s Archiv,” Bd. cn). The stenosis due to pylorospasm is described in chapter IX. The pylorus may become obstructed by a swallowed foreign body that may become lodged in it, by a gall-stone, or a gastrolith. Hypertrophic pyloric stenosis has been considered in a special chapter. Obstruction due to benign tumors is exceedingly rare ; such abnormalities are not discovered except at autopsies. Dr. W. S. Thayer, of the Johns Hopkins Hospital, has related to the writer a case in his experience in which obstruction of the pylorus had been caused by a fibroma. For further information concerning benign tumors, foreign bodies, gastroliths, etc., the reader is referred to chapter vi, of part in. Scar tissue may develop in the neighborhood of the outlet of the stomach as a result of the destructive action of corrosive poison. 658 MOTOR INSUFFICIENCY. This is also a rare occurrence, since chemicals that are swallowed in sufficient quantity to destroy the pyloric tissue would, most prob- ably, cause death by the injury they inflict on the esophagus and portions of the stomach. The outlet of the stomach may be com- pressed by tumors developing in its vicinity, such as pancreatic cysts, malignant tumors of the pancreas, liver, and omentum, fecal concretions in the colon. The lodgment of a large gall-stone in the common bile-duct or in the duodenum has been known to have the same effect. Perigastritis and peritonitis may effect stenosis of the pylorus by constricting bands of fibrous tissue. The author has reported a case of persistent gastralgia in a negro, operated upon on his advice by Dr. John D. Blake. The stomach was bound down to the liver, diaphragm, and transverse colon by numerous adhesions. Those going to the liver had produced an absolute stenosis of the pylorus. Syphilitic and tubercular ulcers (see chapter devoted to this sub- ject) are very rare in the stomach. In one case of tubercular ulceration extending through the pylorus into the duodenum the author found this orifice normally permeable. A number of the causes enumerated may also bring about duodenal stenosis and obstruction, which is often clinically indis- tinguishable from pyloric obstruction. Peptic ulcer may effect constriction of the outlet of the stomach in three ways: (1) The induration inflammatory thickening of the edges of the ulcer may encroach upon the lumen of the pylorus ; (2) the pain and irritation of the ulcer may cause pylorospasm ; (3) in healing the contraction of the cicatrix may effect a deformity of the pyloric canal. The most frequent cause of pyloric obstruc- tion is cancer. From the tables referred to previously, it is evident that ulcer affects the pylorus in 12 per cent, of 793 cases collected by Welch ; and carcinoma occurred in the pyloric region in 60.8 per cent, of 1300 cases of cancer collected by the same author. Symptomatology. — The symptoms of pyloric stenosis may be arranged under three headings — compensation, stagnation, and retention — which represent degrees and phases of the conse- quences of the obstruction. This classification of the symptoms has been ingeniously followed out by Van Valzah and Nisbet (“ Diseases of the Stomach,” p. 584). Not all cases present these three degrees, for whenever the stenosis is malignant, the stage of compensation does not occur. The results of stenosis are familiar SYMPTOMS OF PYLOKIC OBSTRUCTION. 659 from the analogies with stenosis of other hollow muscular organs, such as the heart and the bladder. When the pylorus is nar- rowed, the stagnating ingesta may influence the musculature in two diagonally opposite ways. They may effect a stretching and dila- tation, or constitute an incentive to the gastric musculature bring- ing on increased contraction and peristaltic unrest. The result that will be produced depends upon the state of nutrition of the musculature at the time the stenosis occurs. We exclude malignant tumors as agents causing the increase of gastric musculature by hyperplasia of the normal tissues. If the gastric muscular fiber is well nourished, new formation of muscle-fibers and increased con- traction will result. This constitutes the stage of compensation. But if they are badly nourished, a dilation of the stomach will result, leading to stagnation and retention, so that development of dilation on one hand or hypertrophy on the other, depends largely upon the state of nutrition of the gastric muscle. But if the obstruction persists, which it does as a rule, the distention of the gastric wall and consequent permanent dilation will eventually supervene, although compensation had been for a time established. In case the constriction be moderate and remains so, and overburdening of the gastric wall be carefully avoided, a normal volume of the hypertrophic stomach will persist for a long time. There are three factors that control the advent of stagna- tion and retention — (i) the width of the outlet, (2) the bulk and weight of the ingesta, and (3) the neuromuscular energy of the expulsive force. Thus, stagnation and retention may be caused by gastric atony or myasthenia, because the expulsive force is not sufficient to expel the contents. It may occur after excessive bur- dening of the stomach by ingesta, because the weight on the gas- tric contents is too heavy for the musculature. Hyperacidity and supersecretion may cause stagnation and retention of food by producing a secondary pyloric spasm. The tonic contractions of the pylorus in excessive secretion of acid gastric juice appears to be a precaution to prevent undue acidifica- tion of the duodenal digestive juices. A small quantity of free HC 1 has little or no retarding influence on the diastatic action of pancreatic juice (Rachford), but a very acid gastric chyme renders the ferments of the pancreatic juice inoperative. As a rule, the dilation of the stomach is secondary to the stenosis; but there are very rare and curious cases in which the stenosis is caused by, and secondary to, the dilatation. (See chapter on Motor 66o MOTOR INSUFFICIENCY. Insufficiency.) When distention and dilation have been caused by overburdening the stomach, hypertrophy of the musculature may counteract stagnation and retention ; but if the musculature is incapable of resistance of further development, the overdis- tention of the stomach may distort the lumen of the pylorus, pro- ducing a secondary stenosis. I have reported a number of cases in which the stomach was of normal size when empty, but showed all the evidences of dilation when filled with food. At the opera- tion a rather sharp bend in the duodenum just beyond the pylorus was discovered by the author. This kinking of the duodenum was effected by traction when the stomach was overdistended. Kussmaul (“ Peristalt. Unruhe d. Magens,” Volkmann’s Vortrage, Nr. 1 8 1 ) has described a similar condition in the duodenum pro- duced secondarily by dilated stomachs, and reproduced the ab- normality experimentally in the cadaver. Stenosis of the pylorus, as far as the relation between (i) expulsive power and (2) bulk of gastric chyme are concerned, may be ( a ) absolute or ( b ) relative. (See p. 477.) In such conditions of secondary stenosis, although the constriction may not be absolute, yet it may be relative because it may not suffice for the exit of the large quantity of the gastric contents ; or, again, even when the contents are not excessive, the width of the outlet may be relatively too small for the contractile power of the musculature. Congenital Pyloric Stenosis. — The subject of congenital hy- pertrophic stenosis of the pylorus in infants has been ably reviewed in an article by S. J. Meltzer (“ New York Medical Record,” Aug. 20, 1898), in which he adds a new case to the literature of this sub- ject. A histological examination of the stomach, after the autopsy, was made by T. Mitchell Prudden, showing the thickening of the pylorus to have been largely due to the presence of dense fibrous tissue in the submucosa, and to a hyperplasia of the inner mus- cular layer, especially of the proximal half of the pyloric portion. The moderate thickening of the wall of the gastroduodenal valve, which could be seen as a prominence when viewed from the duo- denal side, was almost wholly due to fibrous hyperplasia in the submucosa. At the proximal end of the pyloric portion the thick- ening was due to increase in the submucosa and inner muscular layer. The external muscular layer presented no abnormality. Like others who have considered this subject, Meltzer divides the life-history of this stomach into three phases — (1) the phase of simple insufficiency, (2) of attempted compensation, and finally (3) CONGENITAL PYLORIC STENOSIS. 66 the phase of atony and dilation. The stomach of this neonatus when completely filled for the first time was not able to empty it- self thoroughly in the interval before the second feeding; only a part of its contents could be evacuated into the intestines. A por- tion remained behind in the stomach, and was present there when the second feeding took place. This same partial retention occur- ring with every feeding finally led to overdistention, which, in turn, evoked the increased contractility of the muscularis, followed by a somewhat greater quantitative expulsion of the contents into the intestine. But as the accumulation of remnants in the stomach had been proportionately greater before this extraordinary mus- cular effort took place, the balance remaining in the stomach was, notwithstanding, greater now than in the foregoing interval. Finally, a stage will come when the muscular fibers make their extremest effort upon the accumulation of the several balances in the stomach ; this extreme effort results in the expulsion of the entire contents by vomiting. This stage is that of insufficiency. The stomach is unable to empty its contents entirely into the in- testine, but it is not yet in a state of dilation. The muscularis still retains its tonicity. The constant overdistention in the method I have previously described causes the development of a varied degree of muscular hypertrophy, which, when once accomplished, causes the stomach to respond even to moderate overdistention with very powerful contraction, so that the entire gastric contents may be expelled through the cardiac orifice. The frequent repeti- tion of this form of evacuation may then bring on insufficiency of the cardia. Frequent vomiting generally starts with the develop- ment of the compensating hypertrophy of the gastric muscularis. The unnecessarily strong contraction effects a partial dilation of the pyloric stenosis in a similar manner as it overcomes the nor- mal contraction of the cardia. It is also instrumental in the ab- normal distention of the fundus, for in this portion the muscularis is very thinly developed, and does not take part in the hypertrophy that is so prominent toward the pyloric end. During the power- ful contraction of the hypertrophied pyloric portion the gastric contents are driven into the fundus, which is incapable of much resistance, and gradually becomes distended and dilated. As it is impossible for the contracting pyloric portion to evacuate all of the chyme, a considerable portion must remain in the most dilatable portion of the stomach. This is the fundus. As the accumulated balances of many feedings become larger and larger, in proportion 44 662 MOTOR INSUFFICIENCY. to the increased size of the fundus, the hypertrophied pyloric end finally exhausts itself in its efforts to overcome the obstruction : it loses its contractility, the muscular fibers may become degener- ated through overexertion, and eventually the third phase, that of gastrectasis, is reached. The body is insufficiently nourished long before this ; in the phase of compensation it begins to suffer, and though with the increased pressure within the stomach a greater transmission of food into the intestine takes place, the amount passed is inadequate for the nutrition of the body. This detailed description of the mechanism of pyloric insuffi- ciency and the consequent stages of compensation and dilation was considered necessary because it represents, in rough outlines, exactly what occurs in every case of pyloric stenosis, excepting, perhaps, those cases due to carcinoma. Here the carcinomatous invasion and the consequent putrefaction and gastrectasis prevent the stage of compensation. Diagnosis. — In the first stage the greediness which the child displays in taking the nursing-bottle and the constant crying should suggest, the possibility of congenital stenosis of the pylorus. A catheter should be introduced into the stomach about two hours after feeding, and the organ evacuated. The amount of the pre- vious feeding must be known. If there is a residual balance in the stomach, it is evident that an insufficiency is present. In the second stage Meltzer places reliance on the following symptoms: The change of the area of percussion with the degree of filling of the stomach ; the appearance of peristaltic waves over the region of the stomach ; palpation of the contracted stomach in an empty state. In the stage of compensated hypertrophy the frequent vomiting immediately after drinking, the absence of vomiting at any other time, the absence of bile from the vomit, and its non- catarrhal appearance are characteristic symptoms. The diagnosis of the last stage, the gastrectasis, should offer no difficulty. The stomach may be filled with air or water, when palpation and percussion will give evidence of the dilation. When air is blown into the partly filled stomach, a gurgling sound can be localized at an abnormally low level by means of the stetho- scope. Simple inspection will reveal the bulging upper part of the abdomen, while the lower part is in a collapsed state. W. Soltau Fenwick (“ Disorders of Digestion in Infancy and Child- hood ”) was able to examine the contents of such an infant TREATMENT OF CONGENITAL STENOSIS. 663 stomach, after a test-meal, and found that the secretion of HC1 was normal. Prognosis. — The disease usually proves fatal within the first three months of infant life, very frequently within a few weeks. Few children having congenital stenosis of the pylorus live to attain adult life. It seems that the disease is not necessarily fatal within itself, but becomes so because it is not recognized. With an early diagnosis and proper treatment the lives of some of these infants might be saved. Four children are on record as having been kept alive by these means — three cases published by Heub- ner (/. c.) and one by Henschel (/. c.). Treatment. — The palliative treatment consists in regulation of the feeding, and frequent washing of the stomach. The advice of Meltzer to give a slightly larger amount of milk than the normal capacity of the stomach in the first stage of the trouble — in order to bring out better contraction of the muscular tissue, and drive more food into the intestines, and thereby effect dilation of the py- lorus — seems to me a doubtful procedure. Overburdening of the gastric walls can do nothing but harm, and the expected increase of muscular contraction may not take place. We can not tell the condition of the nutrition of the muscular layer. Washing the stomach with a one-half of a one percent, solution of Carlsbad salts is recommended by Heubner. A very small piece of tenacious mucus or a coagulum of milk sticking in the pylorus may be suf- ficient to make this passage absolutely impenetrable. Hence the utility of lavage. Massage of the stomach has been recommended. Rectal enemata of milk and egg-albumen will support the strength of the little patient. But the only curative procedure is opera- tion. There have been cases when the infant lived a number of years without operation ; but in view of the rapid advances of gastric surgery, and the positive and permanent relief accruing from a successful gastro-enterostomy, operation should be urged whenever the diagnosis can be clearly established. LITERATURE ON CONGENITAL HYPERTROPHIC STENOSIS OF THE PYLORUS IN INFANTS. 1. Ashby, H., “Archives of Pediatrics,” 1897. 2. Finkelstein, “ Jahrbuch f. Kinderheilk.,” vol. vm, 1896, p. 105. 3. Thompson, “On Congenital Gastric Spasm,” “The Scottish Med. and Surg. Jour.,” 1897. 4. Henschel, “ Archiv f. Kinderheilk.,” vol. xm, 1891, p. 32. 664 MOTOR INSUFFICIENCY. 5. Schwyzer, “ New York Med. Jour.,” 1897. 6. Rolleston and Haynes, “British Med. Jour.,” April 23, 1898, p. 1070. 7. Williamson, “ London and Edinburgh Monthly Jour, of Med. Sciences,” 1841, p. 23. 8. Davoski, “Caspar’s Wochenschrift,” 1842, No. 7. 9. Hirschsprung, “ Jahrbuch f. Kinderheilk.,” vol. xxvm, 1888, p. 61. 10. Gran, “Jahrbuch f. Kinderheilk.,” vol, xliii, 1896, p. 118. 11. Landerer, “ Ueber angeborene Stenose des Pylorus,” Dissert., Tubingen, 1879. 12. Maier, Rud., “Virchow’s Archiv,” vol. cil, 1885, p. 413. 13. Meltzer, S. J., “ N. Y. Med. Rec.,” Aug., 1898. 14. Huebner, Quoted by Finkelstein. 15. Peden, “ Glasgow Med. Jour.,” 1889, p. 416. 16. Pitt, “Trans. Path. Soc.,” London, 1889, p. 63. 17. De Bruin Kops, “ Nederlandsch. Tijdschrift voor Geneeskunde,” 1896, No. 19. (After Thomson.) 18. Thomson, “ Edin. Hosp. Reports,” vol. iv, 1896, p. 116. 19. Schwyzer, “ New York Med. Jour.,” Nov. 21, 1896. 20. Fenwick, “The Disorders of Digestion in Infancy and Childhood,” London, 1897. 21. Loesschaft, “ Jahrbuch f. Kinderheilk.,” vol. xxii, p. 164. 22. Brandt, “ Die Stenose des Pylorus,” Dissert., Jena, 1851. For Obstruction of the Pylorus Caused by Cicatrices, Pep- tic Ulcer, or Carcinoma, see the chapters devoted to these sub- jects. Various Symptoms After Different Causes of Obstruction. — The stages of (1) insufficiency, (2) compensation, and (3) atony and dilation with the attendant stagnation and retention, are present in all forms, except, perhaps, a rapidly developing pyloric carcinoma. In the benign stenoses the first period is generally overlooked ; but dietetic errors bring on attacks of gastric pain of increasing severity, which are generally relieved by vomiting. The vomited food contains, in most cases, more liquid than has been swallowed, which is explained by the investigations of von Mering, who demonstrated that when the stomach contained absorbable substances (alcohol, salts, sugar, dextrin, peptone) and their transition into the intestine is prevented, absorption takes place more or less in the stomach itself, but simultaneously with it an excretion of water occurs into the stomach. This liquid can not find an outlet through the pylorus, and is expelled during the attacks of vomiting. The vomit under such conditions con- tains an abundance of mucus, and often an excess of free and com- bined HC 1 . After the emesis the pain subsides. It may happen EFFECTS OF VARIOUS FORMS OF STENOSIS. 665 that the very next meal may pass the pylorus, because perfect compensation has been established. There is invariably a persistent constipation. At the onset the intermissions between the attacks extend for months, in which there is perfect freedom from pain and vomiting; but as the stage of atony and dilation is ap- proached, the stenosis meanwhile having become more absolute, the attacks occur more frequently, until they finally take place regularly after every large meal. When the period of stagnation has become established, pain is usually present whenever food is taken into the stomach. The vomit gives the chemical evidences, and sometimes also the histo- logical evidences, of gastritis. In the retention of dilation the vomiting is not so frequent, but more copious. The amount of free and combined HC 1 gradually becomes less and less, even when the stenosis is benign ; this is due to the progressing gas- tritis. Now, the conditions favorable to the development of lactic acid are present; these are: (i) Impaired gastric motility; (2) absence of HC 1 ; (3) reduction of albumen digestion; (4) impaired absorption ; and (5) presence of lactic acid bacteria. Acetic and butyric acids are present if the original substances from which they can develop were contained in the food (alcohol-butter). The gastric contents after being drawn separate into three layers ; and if the stenosis is benign, usually contain the products of pepsin digestion. The quantity of urine is small, its amount being in pro- portion to the degree of the stenosis and retention. The appetite is lost, severe cachexia develops, and the case may end fatally if not properly treated. The foregoing is the usual course with a benign stenosis, such as may occur with hypertrophy of the pylorus or benign tumor. The symptomatology after a stenosis due to gastric ulcer may present peculiarities. If an ulcer is located in the pylorus, it may begin with its usual classical signs and symptoms. A stenosis may develop from the inflammatory swelling and induration sur- rounding the ulcer; or, later on, as a result of cicatricial contraction when the ulcer heals. Chronic peptic ulcer still in its progressive stage does not give rise to hemorrhage nearly so frequently as the acute ulcer located in other parts of the stomach. When the obstruction is developed, there is usually vomiting, occurring from one-half to three hours after meals but occasionally containing food taken twelve hours previously. There may be stagnation, retention, and fermentation, as in sten- 666 MOTOR INSUFFICIENCY. osis caused by other benign obstructions. We have observed cases in which the symptoms of vomiting, pain, and retention entirely disappeared after the ulcer was brought to healing by proper treatment. The patients remained apparently cured for a period varying from six months to two years, when the same symptoms and evidences of retention returned, which in a number of our cases were proved to be due to the contracting cicatrix at the operation. Thus, the clinical history of obstruction due to peptic ulcer may extend over as many years as that of hypertrophic stenosis. The Appetite. — The appetite is absent in carcinoma; it is present or exaggerated in ulcer and benign hypertrophy ; as a rule, it will vary with the state of gastric cleanliness. In all conditions when there is much gastric fermentation, the appetite is dimin- ished. Thirst is normal whenever compensation is perfect; but may cause much suffering during retention. Fullness, Distention, Pressure, and Pain. — The overloaded stomach gives rise to a sense of uneasiness. The increased con- tractions during compensation frequently cause distress. The contractions of a hypertrophic or ulcerated pylorus cause severe pain, which becomes most intense when a struggle occurs between the antagonistic contractions of the stomach and pylorus. Nausea and Vomiting. — These symptoms as they occur in gastritis, ulcer, carcinoma, hyperacidity, hypertrophic stenosis, congenital pyloric stenosis, and benign tumors, have been described in the chapters devoted to these subjects. There is nothing in- variably characteristic in the nature and chemical composition of the vomit in these various conditions by which a diagnosis could be arrived at. The chemical differences, as far as they are of diagnostic value, have been described in the chapters referred to. Emaciation, Loss of Weight and Strength. — These are due to the albuminous decomposition brought about by the possible carcinoma, but more frequently by the fact that most of the food is vomited and can not enter the intestine. It is possible that autointoxication may be instrumental in the bodily denutrition. It must not be overlooked that the modern ideas of intestinal autointoxication are nothing but hypotheses, and lack sufficient experimental foundation. That there is some truth in it we do not wish to deny, but much hard and well-directed work is neces- sary before we can admit of the intestinal autointoxication theory as an explanation of malnutrition. SYMPTOMS OF PYLORIC OBSTRUCTION. 667 Tumor. — This subject has been thoroughly ventilated in the chapter on Malignant Neoplasm, and the differentiation of gastric tumors from those of other abdominal organs explicitly stated. It must be emphasized again that when the pylorus is in its nor- mal position, — under the left lobe of the liver, — it can not be pal- pated, even when there is a tumor present. In a case recently operated upon, by the author’s suggestion, by Professor L. M. Tiffany, a pyloric tumor exceeding the size of a man’s fist was firmly attached by adhesions to the under surface of the liver. This large cancerous mass could not be felt because it was firmly held under the liver and out of the way of any possible palpation. The Cause of the Stenosis in the Duodenum. — When gastric retention and dilation are caused by an obstruction in the duo- denum, the exact definition of the diagnosis is difficult. Among the principal causes that act in this manner are: (1) Twisting and torsion of the horizontal part of the duodenum, brought about by partial rotation of the filled stomach when the abdominal walls are very much relaxed (Kussmaul). (2) Indurated ulcers of the duodenum. (3) Carcinoma of the duodenum. (4) Carcinoma of adjacent organs, liver, gall-bladder, pancreas, colon, omentum. (5) Gall-stones projecting into the lumen of the intestine, and act- ing directly as an obstruction, or by causing an adhesive and stenosing inflammation. In a case described by Mikulicz in which the stone was removed by gastrotomy, this inflammatory indura- tion had occurred immediately below the pylorus. Among the causes that act externally to the duodenum we should mention also, in addition to the tumors of the neighboring organs referred to, enlarged lymph-glands in the mesentery. (6) Cicatricial adhe- sions after round ulcer, or purulent gastritis, or former inflamma- tions of the peritoneum, such as pericolitis, or appendicitis. (7) Traction and distortion of the duodenum and pyloric region, induced by large herniae, especially scrotal (Rokitansky). It is very doubtful whether right-sided floating kidney can com- press the duodenum sufficiently to produce gastrectasis, and Leube, Ewald, Oser, Nothnagel, and Kuttner have advanced convincing arguments against such an assumption. This error was probably due to the confounding of dilation or gastrectasis with atony and particularly with gastroptosis. These are affections that occur simultaneously with floating kidney, and are probably due to com- mon causes, such as relaxation of the abdominal muscles, stretch- ing of the peritoneal folds known as ligaments. I agree with 668 MOTOR INSUFFICIENCY. Riegel that gastroptosis is not rarely combined with gastrectasis, but the cause of this by dislocated kidney is not proved ; it is conceded, however, that a dislocated right kidney which has become fixed in its abnormal position, or a kidney that has in- creased enormously in size may compress the duodenum and cause a dilation. A definite decision concerning the various causes that may lead to obstruction of the pylorus is very frequently not possible, although every attainable diagnostic moment is considered care- fully. With the status of our present knowledge of diseases of the stomach it is impossible to recognize the beginning of pyloric stenosis with precision, and the practitioner will have to be content if he is enabled to decide whether the dilation and retention are due to a malignant or to a benign process. In the writer’s experi- ence all further deductions made from the clinical phenomena con- cerning the particular nature and origin of the many possible varieties of benign stenosis are largely conjectural. The differen- tial points between benign and malignant pyloric stenoses have been given in the chapters on Carcinoma, Ulcer, and Hypertrophic Stenosis ; but for the sake of convenience, we will briefly recapitu- late them here. 1. Age. — Refer to the tables already stated. Malignant tumors occur at a more advanced age, but it must not be overlooked that the age of carcinomatous patients is receding, and that malignant tumors may occur at a very youthful age; therefore this moment is of not much utility in the diagnosis. 2. Duration. — Benign stenoses last for many years; malignant processes are short, generally from three to six months, only exceptionally exceeding one year. 3. Course and Progress. — In benign stenosis these are very variable. Periods of tolerable well-being or even of good health alternate with periods of severe sickness ; but in malignant steno- sis the aggravation of the symptoms is progressive and continuous, notwithstanding rational treatment. 4. Tumor. — The most important deciding element for the diag- nosis of pyloric stenosis will be the demonstration of a tumor, but in the differentiation between benign stenosis and carcinoma the existence of tumor is of little value. A tumor, if present, may as well be a benign hypertrophy as cancer ; and if it is absent, it does not exclude the diagnosis of either of these conditions. RELATIVE VALUE OF DIAGNOSTIC FACTORS. 669 5. Metastases. — If these can be palpated in other abdominal organs, — for instance, in the liver or in the mesenteric glands, — we have a strong evidence in favor of malignant process. The same may be said of swelling of the cervical lymph-glands occurring in the left supraclavicular region. This complication is, in our ex- perience, a rare occurrence. 6. Edema. — If other causes that may bring on edema of the ankles may be excluded, the presence of this symptom is sugges- tive of a malignant process, but absence of this symptom does not argue against carcinoma. It is a late symptom. 7. Hematemesis. — In my experience blood is contained in the vomit in one-half of all cases of gastric cancer. Large quantities of blood are rarely vomited, but the characteristic cofifee-ground vomit, in consequence of stagnation and decomposition of the blood, is diagnostically important. The more copious the effu- sions of blood into the stomach, the quicker do they cause vomit- ing; for that reason the abundant hemorrhages in ulcer are often vomited uncoagulated and very little altered, whereas the smaller amounts of blood in carcinoma and gastritis remain in the stomach a longer time, and then show the characteristic coffee-ground ap- pearance. But large hemorrhages may occur in cancer, and small hemorrhages may occur in ulcer ; and I have seen cases of coffee- ground vomiting in ulcer repeatedly. 8. Chemistry of the Gastric Contents. — This has been dwelt upon in the chapters on Ulcer and Carcinoma. Hyperchlorhydria or hyperacidity is suggestive of a cicatrix or cicatricial tumor formed from an ulcer. It also occurs in the ulcus carcinoma- tosum, the carcinomatous degeneration of the peptic ulcer. Ab- sence of free HCl may be present in benign as well as malignant stenosis. Pepsin and chymosin are present in the benign cases, but show a very variable condition proportionate to the degree of destruction of the mucosa in malignant conditions. 9. Lactic acid is very rare in benign stenosis, and was present in eighty-two per cent, of all cases of gastric cancer coming to the author’s clinic. It is a valuable though not an early diagnostic sign . 10. Hydrogen Sulphid. — This is said to occur frequently in benign, and rarely in malignant, stenosis. In the author’s opinion this sign is not reliable. 11. Bacteriological Evidences. — These organisms were present in fifty-three out of fifty-five cases of gastric carcinoma, and are of great diagnostic significance. In our experience they have not been 6yo MOTOR INSUFFICIENCY. found in benign stenosis, though Lindner and Kuttner assert that they do occur in such. Sarcinae occur more frequently and in greater abundance in the benign stenosis. 12. The presence of large numbers of cells in a state of atyp- ical mitosis is, in the writer’s opinion, diagnostically important. We have not been able to find them in the contents of eighteen cases of gastric ulcer and a much larger number of cases of chronic gastritis, which were especially examined with regard to this factor. The study of karyokinesis in cells obtained from the human stomach is as yet very incomplete. It should be carried out in a large number of gastric diseases other than cancer. Cells in a state of atypical mitosis are early signs of cellular proliferation, and very suggestive of malignant disease. So far, very few cases of gastric cancer have been diagnosed by this method. 13. Fragments of Neoplasm. — While these clinch the diag- nosis of carcinoma, they are not early signs. If they are found in the wash-water without any special effort having been made to de- tach them, they come from tumors that are in a state of disinte- gration, and, in my experience, often were found to have already induced glandular metastases. The differential diagnosis between benign and malignant stenoses is not always clear, even after a pyloric tumor can be palpated. But when no tumor can be palpated, judgment is, indeed, difficult, and is possible only after frequent and prolonged observations ; in rare instances, in the author’s experience, the diagnosis could not positively be made even after exploratory laparotomy. The differential diagnosis between motor insufficiency due to obstruction and that due to myasthenia can be decided in favor of the former whenever a tumor can be palpated. All symp- toms of stagnation, retention, etc., have no differentiating value ; neither has the chemistry of the stomach in the two conditions. These and other distinguishing points are given in the chapter on Motor Insufficiency. The author has devised a method by which a tube can be passed from the mouth through the stomach and py- lorus into the duodenum (Hemmeter, “ Intubation des Deode- num,” Boas, “ Archiv f. Verdauungskrankh.,” Bd. 11, Seite 85 ; see first part of this volume). This method is, in a fair proportion of the cases, available for the determination for the permeability of the pylorus. Similar methods have been described by Dr. Fenton B. Turck and F. Kuhn. Efforts of this kind to sound the pylorus give promise of diagnostic aid and of enlarging the means of treatment. CONTINUED SUPERSECRETION AND PYLORIC OBSTRUCTION. 67 I Hyperacidity, whenever it prolongs gastric digestion and causes distention, does so by causing indigestion of the carbohydrates, or reflex spasm of the pylorus. In simple hyperacidity these symp- toms can be relieved by internal use of the alkalies, or washing the stomach with alkaline solutions. In retention due to obstruction the alkaline treatment will give no benefit. As a rule, in our ex- perience, the motility of the stomach is well preserved in hyper- acidity. Continued Supersecretion and Pyloric Obstruction. — Gastro- succorrhea chronica and dilation of the stomach occur together very frequently. This dilation may be of the so-called atonic or myasthenic variety, or it may be due to pyloric obstruction ; but there are dilations without chronic continued supersecretion, and, on the other hand, this secretory anomaly may, according to Riegel and Reichmann, occur without dilation. The origin of the atonic dilation from a continued supersecretion of gastric juice is ex- plainable by the following facts : The permanent presence of gas- tric juice, the acidity of which may increase with every addi- tion of food, constitutes an inhibition to carbohydrate digestion. The starchy foods are retained abnormally long. Then, again, if a continued secretion of gastric juice is assumed, the stomach, of course, is never entirely empty, and therefore never obtains abso- lute rest, and, finally, the hyperacid contents may cause a pyloric spasm, preventing the exit of the gastric chyme. In this manner gastrosuccorrhea may cause obstruction and retention. Reversely, pyloric stenosis may keep up a kind of continued gastric flow by holding back the food within the stomach. It is almost impossible to decide in such cases whether the pyloric stenosis was primary, or whether it was superadded to an already existing continued supersecretion. The author has been able to observe a number of cases from their very incipiency, and concludes that both varieties occur clinically. Even among those who devote special attention to the abnormalities of secretion there is confusion with regard to the terms hyperacidity and hyperchlorhydria on the one hand, and chronic continued supersecretion and gastrosuccorrhea on the other. We may have retention and dilation together with hyper- acidity ; we may even have a pyloric stenosis together with hyper- acidity ; and yet there will be no sign of chronic continued secre- tion. Hyperacidity means an increased secretion of gastric juice, or rather of HC1, during digestion. The stimulus to this increased secretion is the normal presence of food in the stomach. Hyper- 672 MOTOR INSUFFICIENCY. secretion or continued secretion of the gastric juice is an abnormal condition in which the gastric mucosa secretes continuously, even when the digestive stimulation is absent and the stomach contains no food. This condition may be intermittent and periodical, or it may be continuous. It is a generally accepted fact that hyperacidity predisposes to gastric ulcer, but continued hypersecretion renders a patient much more liable to the development of ulcer than hyperacidity, since in the continued secretion the stomach is never free from gastric juice which is as highly acid as that which occurs in hyperacidity. The development of dilation from continuous hypersecretion may be explained by the presence of an ulcer in the pylorus, which may have resulted in the formation of' a stenosing cicatrix. Thus, a primary continued secretion may give rise to an ulcer, cicatricial stenosis, and a consequent secondary dilation. Hyperacidity represents a lesser degree of irritation, and con- tinued secretion a higher, more intensely irritated state of the se- creting gland-cells. Undoubted cases have occurred in which hyperacidity was intensified and developed into chronic continued hypersecretion. In the cases in which the dilation and reten- tion was the primary condition and the hypersecretion was recog- nized later on, it is not absolutely certain that the dilation caused the hypersecretion; undoubted and long-observed cases of this char- acter, with careful and repeated chemical and physical analyses, have, in our experience, not been published. It is more rational to assume that in such cases the dilation was consequent upon an ulcer in the pylorus, which ulcer had arisen on the basis of a pro- longed hyperacidity. After the dilation had developed, the hy- peracidity was intensified into a chronic continued hypersecretion. A pronounced stagnation of the ingesta consequent upon a dila- tion may very much resemble a continued hypersecretion. To distinguish between these two conditions, it is necessary to examine and analyze the gastric contents in the morning before any food has been taken. In continued secretion the jejune stomach should always contain active gastric juice in quantities from 150 to 300 c.c. This gastric juice should be free from food remnants. This can not occur in simple dilation — it should not even occur in dilation with hyperacidity, for in both of these cases we will find food remnants, particularly undigested carbohydrates. The diagno- sis between the two conditions can be definitely settled by washing out the stomach thoroughly — until the lavage water comes out TREATMENT OF PYLORIC OBSTRUCTION. 673 absolutely clear and shows no signs of acid. This must be done in the evening. The patient must not eat anything in the mean while. The next morning, before food is taken, the gastric contents are drawn by the expression method, and if 100 c.c. or more of gastric juice without any traces of food remnants can be gained, it is a case of continued hypersecretion. The differentiation between dilation with continued hypersecretion or supersecretion and dila- tion with simple hyperacidity hinges upon the presence or absence of food in the stomach when it is prepared as just described. If the presence of food is necessary to bring out the secretion of gastric juice in the stomach in the morning, it is a dilation with hyperacidity; but if the stimulus of food is not necessary, it is a dilation with continued hypersecretion. The degree of the obstruction can be determined by the amount of our double test-meal, or of the test-meals of Herschell, Riegel, or Leube, that remains in the stomach after a certain time. During compensation the stomach succeeds in emptying itself in perhaps one hour longer than the normal time. During stagnation the stomach requires from six to eight hours to empty itself of a Riegel dinner; but when the stagnation is advanced, the stomach is not empty except perhaps before breakfast. In retention the stomach is never empty. The degree of the retention can be measured by the methods given in the chapter on Motor Insuffi- ciency. In benign stenosis the degree of the obstruction may be gaged by the author’s method of duodenal intubation. Prognosis. — The prognosis will vary with the cause. It is grave in malignant obstruction ; and even in benign obstruction, such as peritonitic adhesions, ulcer of the duodenum, impacted gall-stone, corrosive gastritis, etc., the prognosis is grave. If the stenosis is due simply to kinking of the pylorus or duodenum by a primary atonic dilation, the prognosis is also bad, because not even surgical aid can be depended upon to relieve this condition permanently. Treatment. — The maxim of all treatment in these cases should be : “ In pyloric obstruction beware of wasting valuable time with purely medical treatment.” The medical treatment is given in the chapter on Motor Insufficiency. It is very much to be regretted that the literature of the subject shows no well-observed cases in which undoubted benign stenosis was cured by purely medical means. The plan that promises the best results is to decide rapidly upon an operation, exclude all medicines and food from the stomach, maintain the patient’s strength by rectal alimentation, 674 MOTOR INSUFFICIENCY. and administer ^ of a grain of strychnin hypodermically four times a day. During the period of complete compensation, par- ticularly if the obstruction is benign, the patients will rarely con- sult the physician. During this stage, when the periodical attacks of vomiting and stagnation begin, the diet should be that of motor insufficiency of the first degree. It is very difficult to convince the patient of the necessity of operation during this stage, and even during the stage of stagnation. The physician is unfortu- nately, therefore, frequently compelled to persist in purely medical treatment, notwithstanding his convictions to the contrary. Lavage . — I prefer to carry out lavage during stagnation in the evening, according to Riegel’s plan. The last meal is given be- tween four and five o’clock in the afternoon, consisting of some food that will readily pass the pylorus, even though it may be par- tially constricted. Milk, koumiss or matzoon, the whites of four eggs, egg beaten up in hot beef bouillon with four grams of soma- tose added, custard, meat pulp, cream, Zwieback or cake, cerealin, strained oatmeal, strained breakfast wheat, well-boiled rice, soft- boiled eggs, corn-meal mush, are suggested as possible articles of diet. Great solubility and fluidity of the food, and minute sub- division in its preparation are desiderata in the process of cooking. Whenever possible, the food should be strained or passed through a colander. Soup made of sweetbread in beef bouillon has a high caloric value. After such a meal the patient must lie down and submit to gastric massage. With this aid, and in the recumbent position, the liquid diet is, as a rule, out of the stomach in five hours ; if it is not, there is no need of further experimentation with dietetic and medicinal treatment. After the meal can be presumed to be out of the stomach, the organ is thoroughly washed out with medicated solutions that are varied according to the condition of the gastric chemistry. If no HC 1 is present, it is well to use first sodium chlorid, one teaspoonful to the quart of warm water, and toward the end of the operation a solution of dilute HC 1 , say a 3 to 4:1000 solution. If the gastric contents show persistent hyperacidity, I prefer to wash out the stomach with sodium bi- carbonate, one teaspoonful to the quart, followed by a solution of nitrate of silver, 1 : 1000, or a one-half of one per cent, solution of tannin. If gastric ulcer is suspected, a suspension of subnitrate or subgallate of bismuth may be used with advantage, one dram to the quart of warm water, and permitted to run in during constant agitation of the suspension of the bismuth. LITERATURE. 675 In addition to fine subdivision of the food, the next most im- portant dietetic principle is to assure one’s self that the stomach is always empty before a meal is permitted. To ascertain this, it is necessary to learn the time in which the patient’s stomach will evacuate itself, by passing a stomach-tube from four to five hours after a meal like the Riegel dinner, or by employing our double test-meal. The stool should be watched and sufficient food introduced to cover the caloric requirements of the patient. It is not an easy matter to gage the proper amount of food to be introduced into these weak stomachs. The danger of overburdening is very great. It is, therefore, advisable to give two, perhaps three, nutri- tive enemata a day, which will permit of considerable reduction in the amount of food necessary to be given by the mouth. Dilation of Benign Pyloric Stenosis by Sounding. — This method has been employed by the author in obstruction due to hyper- trophic stenosis of the pylorus, when operation was refused. The cases were markedly relieved for a time, but permanent cure of the obstruction by this method seems doubtful. Nevertheless, the technics of this procedure should be perfected to be available in the efforts to dilate cicatricial and hypertrophic stenosis whenever operation is impossible or refused. (Concerning the indications and methods of operation, see the chapter devoted to Surgery of the Stomach, or the Cartwright lectures on “ Surgery of the Stomach,” by W. W. Keen, LL.D., “ Philadelphia Medical Jour- nal,” volume 1, pages 829, 927, 1053, an d 1104.) LITERATURE ON DILATION OF THE STOMACH. 1. Abrams, A., “ Gastrectatic Dyspnea,” “Pacific Rec. M. and S.,” San Francisco, 1898-’ 99, xm, 39-42. 2. Alex, “ Stenose du pylore d’origine biliaire,” “ These de Lyon,” 97. 3. Anderson, “British Med. Jour.,” May 10, 1890. 4. Von Anrep, “Du Bois’ Archiv,” 1881. 5. Armstrong, W., “Gastric Dilation,” “Brit. Med. Jour.,” Lond., 1898, I, 949. 6. Ashby, H., “A Case of Congenital Stenosis of the Pylorus,” “Arch. Pediat.,” New York, 1897, xiv, 498-505. 7. Aufrecht, “ Centralbl. f. klin. Med.,” 1893, Nr. 23. 8. Bardet, “ Bull. Gen. de Therap.,” 1884, 329. 9. Bartels, “ Berl. klin. Wochenschr.,” 1877, Nr. 30. 10. Von Basch, “Berl. klin. Wochenschr.,” 1889, Nr. 19, S. 433. 6y6 MOTOR INSUFFICIENCY. 11. Bauermeister, I naug.- Dissert., Halle, 1890. 12. Baum, “Wien. med. Presse,” Nr. 17, 1873. 13. Beau, “ Gaz. Med. de Paris,” No. 5, i860. 14. Beaumetz, D., et D. Ettinger, “ Union Medicale,” 29 Janvier, 1884. 15. Beaumont, “ Experiments on the Gastric Juice,” 1838. 16. Benedict, A. L., “ Diagnosis of the Gastric Conditions Producing Ischo- chymia (Atony, Gastroptosis, Atonic Dilation, Obstructive Dilation),” “ Med. Age,” Detroit, 1898, xvi, 386-392. 17. Beurmann, “Gaz. Hebd.,” No. 14, 1889. 18. Bettmann, H. W., “Acute Dilation of the Stomach,” “Cincin. Lancet- Clinic,” 1897, N. S., xxxviii, 569-575. 19. Bettmann, H. W., “Motor Insufficiency of the Stomach,” “Cincin. Lancet-Clinic,” 1897, xxxviii, 517-522, Discussion, 525; also, “ Tr. Acad. Med.,” Cincin., i 897 ~’ 98 . 20. Bircher, H., “ Correspondenzbl. f. Schweizer Aerzte,” 1891, Nr. 23. 21. Boas, “ Diagnostik u. Therapie der Magenkrankheiten,” 2. Theil, S. in, Leipzig, 1893. 22. Boas, “Deutsche med. Wochenschr.,” 1893, Nr. 39, und “ Miinchener med. Wochenschr.,” 1893, Nr. 43. 23. Boas, “ Hypertrophic Stenosis of the Pylorus and jts Treatment,” “ Arch, d. Verdauungskrankh.,” Apr. 1, 1898. 24. Bokai, A., “ Wirkung des Quassin betr.,” “ Pester med.-chirurg. Presse,” 1893, Nr. 45. 25. Bouveret, “Stenose du pylore adherent a la vesicule calculeuse,” “Revue de Med.,” Jan., 1896. 26. Bouveret, “ Sur le diagnose de l’estomac biloculaire par l’insufflation,” “ Lyon Medical.,” 2, 11, 1896. 27. Bouveret et Devic, “ Revue de Medec.,” 1892, H. 1 und 11. 28. Boyd, M. A., “ A Clinical Lecture on the Significance of Dilation or Gastrectasia in Functional and Organic Diseases of the Stomach,” “ Brit. Med. Jour.,” London, 1897, II, 265, 266. 29. Broadbent, W. H., “Dilation of the Stomach,” “Practitioner,” Lon- don, 1898, lx, 11-28. 30. Brown, R. Hill, “Case of Dilation of the Stomach Complicated by Fatal Tetany,” “ Lancet,” 21, in. 31. Bruhl, “Gaz. des Hopitaux,” 1891. 32. Bugge, “ Tidshrift f. pract. Med.,” Nr. 10, 1881. 33. Buist, S. Somers, “ Amer. Jour, of Med. Sciences,” Oct., 1870. 34. Carr, W., “ A Case of Dilation of the Stomach Associated with Per- ipheral Neuritis,” “ Lancet,” London, 1897, 11, 721. 35. Carrel, “ L’estomac biloculaire (presentation de la piece),” Soc. des Science Med. de Lyon, Mai, 1896. 36. Cautley, E., “Congenital Hypertrophic Stenosis of the Pylorus,” “Lancet,” London, 1898, 11, 1264. 37. Cecchini, S., “ Rassegna di Scienza mediche,” 1886. 38. Chauffard, “ Stenose pylorique; gastroenteroanastomose, etat du malade trois mois apres l’operation, Presentations de malade,” Soc. Med. des Hop., 22 Oct., 1896. 39. Chauffard, A., “Stenose pylorique et vaste dilatation de l’estomac ; LITERATURE. 677 application au diagnostic de l’6clairage 61ectrique intra stomacal,” “ Bull, et Mem. Soc. Med. d. Hop. de Par.,” 1897, 3 S., xiv, 979-982. 40. Chiari, “ Wiep. med. Blatt,” Nr. 3, 1881. 41. Chomel, “ Des Dyspepsies,” Paris, 1857. 42. Comby, J., “Dilatation de l'estomac chez les nourrissons,” “Bull, et M6m. Soc. M6d. d. Hop. de Par.,” 1897, 3 S., 850-857. 43. Comby, “Dilatation de l’estomac chez le enfants,” Soc. Med des Hop., 18 Juin, 1897. 44. Comby, “Arch. Gen. de Med.,” Aout, 1884. 45. Cordier, A. H., “ Gastro-jejunostomy in Gastrectasis,” “Med. Record,” 25, ix, 1897. 46. Coyon, A., “ Stenoses du pylore,” “ Gaz. d. hop.,” Paris, 1898, lxxi, 9 1 7 > 945- 47. Debove, Soc. Med. des Hopit., 12 Dec., 1886. 48. Dehio, “ Verhandlungen d. Cong. f. innere Med.,” 1888. 49. Deiters, Inaug.-Dissert., Greifswalde, 1889. 50. Donkin, “The Lancet,” Sept. 27, 1890. 51. Duchon-Doris, “These de Paris,” 1887. 52. Dujardin-Beaumetz, “ Berl. klin. Wochenschr.,” 1890, Nr. 31. 53. Dunin, “ Resultate der Gastroenterostomie bei narb. Pylorusstenose,” “ Centralbl. f. Chirurg.,” 1893, Nr. 36. 54. Einhorn, V., “ Ueber elektr. Magen- und Darmdurchleuchtung,” “ Therap. Monatshefte,” 1892, S. 128. 55. Einhorn, “ Berl. klin. Wochenschr.,” 1891, Nr. 23. 56. Einhorn, M., “A Further Contribution to our Knowledge of Ischochy- mia,” “ Med. Rec.,” New York, 1877, li, 865-873. 57. Erdmann, “Virchow’s Archiv,” Bd. xliii, S. 295. 58. Ewald, “Berl. klin. Wochenschr.,” 1890, Nr. 12. 59. Ewald, “Therap. Monatshefte,” August, 1887. 60. Fagge, Hilton, “ Guy’s Hosp. Rep.,” xvm ; “ Virchow’s Jahresb.,” 1873, B. H., S. 155. 61. Fleiner, “ Ueber die Behandl. einiger Reizerschein. u. Blut. des Magens,” “Verhandlungen d. Cong. f. innere Med.,” 1894, S. 309. 62. Francois, L., “ Sur une volumineuse dilation stomacale,” “ Marseille Med.,” 1897, xxxiv, 372-374. 63. Francon, “Lyon Med.,” 7 Aout, 1887. 64. Von Frankl-Hochwart, “ Die Tetanie,” Berlin, 1891. 65. Friedenwald, J., “ Two Interesting Cases of Dilation of the Stomach,” “ Maryland Med. Jour.,” Baltimore, 1897 -’98, xxxvm, 1 53—1 55. 66. Galliard, Assoc. Fran9aise, Congres de Rouen, 1883. 67. Galvagin, E., “ Gastrectasia da stenosi pilorica,” “ Gazz. d. osp.,” ' Milano, 1898, xix, 777-779. 68. Garcia, E. L., “ Dilatacion del estomago sin estinosis pilorica,” Cron, med. Lima,” 1897, xiv, 393 ; 41 1, 1898 ; xv, 6, 25, 61. 69. Garcia, Duarte R., “ De la gastro-ectasia,” “ Gac. med. de Granada,” 1898, XVI. 70. Gerhardt, “ Berl. klin. Wochenschr.,” S. 74, Januar, 1888. 71. Gillet, A., “ Dyspepsie et dilatation gastro-intestinale chez d’enfant,” “ Rev. gen. de Clin, et de Therap.,” Paris, 1897, xi, 325-327. 45 6yS MOTOR INSUFFICIENCY. 72. Grundzach, “Wien. med. Presse,” Nr. 28, 1891. 73. Hamill, S. McC., “Dilated Stomach from Pyloric Obstruction; Con- tracted Kidneys,” “ Tr. Path. Soc. of Phila.,” 1898, xviii, 75-78. 74. Hayem, G., “ Note sur les variations de la capacite stomacale dans les stenoses pyloriques, ” “ Bull, et Mem. Soc. Med. d. Hop. de Paris,” 1897, 3 S., xiv, 1322-1325. 75. Hayem, “ Stenose pylorique,” “ Presse Med.,” 20 Novembre, 1897. 76. Hayem, “ Stenose sous pylorique incomplete.,” “Med. Moderne,” 9 fevrier, 1898. 77. Heynsius, “Weekblad van het Nederlandsch. Tydschrift voor Genesk.,” Nr. 37, 1874. 78. Hirschberg, “These de Paris,” 1889. 79. Hochenegg, J., “A Case of Hour-glass Stomach Cured by Gastroanas- tomosis,” “Wien. klin. Wochenschr.,” July 16, 1898. 80. Hofmann, “ Anzeiger d. Ges. d. Aerzte in Wien,” Nr. 12, 1881. 81. Hoppe-Seyler, “Deutsches Archiv f. klin. Med.,” Bd. l, C. S. 82. 82. Huber, “ Deutsches Archiv f. klin. Med.,” Bd. xlvii. 83. Hufschmidt, “Wien. klin. Wochenschr.,” 1893, Nr. 3. 84. Hunter, “New York Med. Record,” p. 273, 1889. 85. Jacobson und Ewald, “ Ueber Tetanie,” “ Verhandlungen d. Congr. f. innere Medizin,” 1895, S. 298. 86. Jago, “ Med. Times and Gaz.,” Oct. 12, 1872. 87. Jaworski, “Wien. med. Wochenschr.,” No. 16, 1888. 88. Jobin, A., “ Un cas de dilatation aigue de l’estomac,” “ Rev. Med.,” Quebec, 1897, 1, 177. 89. Von Johann, Peter Frank, “ De cur. horn. morb. epit.,” lib. V, pars. 6, p. 666. 90. Jiirgensen, Th. v., “ Tod unter schweren Hirnerscheinungen bei hoch- gradiger Erweiterung des Magens,” “ Archiv f. klin. Med.,” Bd. lx, p. 327. 91. Kansche, “ Unters. fiber die funkt. Resultate von Operat. am Magen.” 92. Kelynack, T. N., “ Gastrectasis Secondary to Malignant Stricture of the Pylorus,” “Med. Press and Circ.,” London, 1898, N. S., lxv, 5. 93. Kern, Inaug.-Dissert., Berlin, 1891. 94. Klemperer, “ Ein Fall geheilter Magenerweiterung,” “ Deutsche med. Wochenschr.,” 1889, Nr. 9. 95. Krasnobayeff, T. P., “ Three Cases of Stricture of the Pyloric Portion of the Stomach in Childhood,” “ Dietsk. med. Mosk.,” 1898, ill, 195-204. 96. Kuckein, R., “A Case of Latent Tetany, with Dilation of the Stomach, in Consequence of Carcinomatous Stenosis of the Pylorus,” “ Berl. klin. Wochenschr.,” Nov. 7, 1898. 97. Kuhn, “ Zeitschr. f. klin. Med.,” 1892, Heft 5 u. 6. 98. Kuhn, “ Deutsche med. Wochenschr.,” 1892, Nr. 49 u. 52. 99. Kussmaul, “ Zur peristalt. Unruhe des Magens,” “Volkm. klin. Vor- trage,” Nr. 181. 100. Kuttner und Jacobson, “ Berl. klin. Wochenschr.,” 1892, Nr. 39 u. 40. 101. Landau, “ Die Wanderniere der Frauen,” Berlin, 1881. 102. Landerer, Inaug.-Dissert., Freiburg, 1879. 103. Laprevotte, “These de Paris,” 1884. 104. Lefevre, “ Archiv Gen. de Med.,” tome xiv et xv, 1842. LITERATURE. 679 105. Leichtenstern, “ Ziemssen’s Handbuch,” 2. Aufl., Bd. vn, 2, S. 411- 418. 106. Leo, “ Diagn. der Krankh. d. Verdauungsorgane,” p. 41, Berlin, 1892. 107. Lepoil, " Th&se de Paris,” 1881. 108. Leube, “ Archiv f. klin. Med.,” Bd. xvm, S. 207. 109. Lindemann, E., “ Demonstration von Rontgenbildern des normalen •und erweiterten Magens,” Deutsche med. Wochenschr.,” 1897, xxm, 266. no. Litten, “ Verhandlungen des VI. Congr. f. innere Med.,” 1887. hi. Lyman, H. M., “Dilation of the Stomach,” “Jour. Amer. Med. Assoc.,” 1897, xxviii. 1 1 2. Maier, R., “Congenital Pyloric Stenosis,” “Virchow’s Archiv,” Bd. cii. 1 13. Malibran, “These de Paris,” 1885. 1 14. Marten, “Lancet,” April 2, 1890, p. 230. 1 1 5. Mattheides, Inaug. -Dissert., Erlangen, 1890. 1 16. Maynard, E. F., “Chronic Dilation of the Stomach Associated with Chronic Gastric Catarrh,” “ Brit. Med. Jour.,” London, 1898, II, 1126. 1 17. Mazotti, Luigi, “ Rivista Clinica di Bologna,” Aout et Sept., 1824. 1 18. McKendrick, John S., “ Case of Tetany with Dilation of the Stomach ; Death,” “ Lancet,” Sept. 24, 1898. 1 19. McNaught, “Dilation and Eructation of Inflammable Gas,” “Brit. Med. Jour.,” 1890. 120. Von Mering, “ Ueber die Funktion des Magens,” “ Verhandl. d. Congr. f. innere Med.,” 1893. 121. Meltzer, S. J., “On Congenital Hypertrophic Stenosis of the Pylorus in Infants,” “Med. Rec.,” New York, Aug. 20, 1898. 122. Meyer, “Virchow’s Archiv,” Bd. cxv, S. 326. 123. Michalis, Walter, “Ueber die Erweiterung des Antrum pylori und ihre Beziehung zu der motorischen Insufficienz des Magens,” “ Zeitschr. f. klin Med.,” Bd. xxxiv, S. 241. 124. Moncorvo, Rio de Janeiro, broch., 1883. 125. Montaya, “These de Paris,” 1881. 126. Montprofit, “Obstruction du pylore par un calculi biliare,” “ Soc. anat. Bullet.,” de Mai-Juin, 1897. 127. Monyour, “Dilatation de l’estomac par stenose du pylore; gastro- enterostomie par le procede G. Dubourg, guerison,” Soc. d’Anat. et de Phys. de Bordeaux, 4 Octob., 1897. 128. Moritz, “Gastric Motility with Regard to Liquids and Semi-liquids,” “Verhandl. d. Naturforsch.-Versamml.,” Wien, 1894. 129. Muller, F., “ Charite Annalen,” p. 283, 1888. 130. Mueller-Warnek, “ Berl. klin. Wochenschr.,” Nr. 30, 429, 1877. 1 31 . Naunyn, “ Gastric Fermentation and Motor Insufficiency,” “ Deutsch. Arch. f. klin. Med.,” Bd. xxxi, 82. 132. Nauwerk, D., “ Archiv f. klin. Med.,” Heft 5 u. 6, vol. XXI, p. 573, 1878. 133. Neumann, “ Deutsche Klinik,” Nr. 2 u. 3, 1861. 134. Newmann, “ Lancet,” Dec. 5, 1868. 135. Oppolzer, “ Magenerweiterung,” “Wien. med. Wochenschr.,” 1893. 136. Oser, Artikel, “Magenerweiterung” in Eulenburg’s “ Realencyclo- padie.” 68o MOTOR INSUFFICIENCY. 137. Pacanowski, “ Zur physikal. Diagnostik d. mechan. Insuff. d. Magens.” 138. Parker, R., “A Series of Operations for Dilated Stomach,” “ Liverpool Med.-Chir. Jour.,” 1898, xvm, 274-282. 139. Patek, A. J., “Atony of the Stomach,” “ Med. News,” New York, 1898, LXXIII, 584-587. 140. Penzoldt, “ Die Magenerweiterung,” Erlangen, 1875. (History of the subject.) 141. Penzoldt (in Penzoldt und Stintzing’s “ Handbuch d. speciellen Ther- apie innerer Krankheiten,” Bd. iv). 142. Penzoldt-Faber, “Berl. klin. Wochenschr.,” 1882, Nr. 21. 143. Pepper, “ Phila. Med. Times,” May 1, 1871. 144. Pepper, W., and Alfred Stengel, “ Diagnosis of Dilation of the Stom- ach,” “ Amer. Jour. Med. ’.Sciences,” Tan., 1898. 145. Perret, “ L’estomac biloculaire,” “ These de Lyon,” 1896. 146. Pertick, “ Archiv f. path. Anat. u. Phys.,” cxiv, 1888, Heft 3, S. 98. 147. Petriquin, “ Bulletin de Therap.,” X, p. 239. 148. Phaundler, M., “ So-called Congenital Stenosis of the Pylorus and its Treatment,” “Wien. klin. Wochenschr.,” Nov. 10, 1898. 149. Plempius, et suivants, cites par D. Beaumetz, “ Traitement des mal de PEstomac,” Paris, 1893. 150. Poensgen, “ Motor- Verricht. d. menschl. Magens,” Strassburg, 1882. 1 5 1. Pope, C., “A Clinical Lecture on Gastric Dilation,” “Charlotte, N. C., Med. Jour.,” 1897, xi, 171-176. 152. Popoff, “ Berl. klin. Wochenschr.,” 1870, Nr. 38 u. 40. 153. Preble, R. B., “ Gastrectasis, with a Tetanoid Condition and the So- called Pulmonary Hypertrophic Osteoarthritis of Marie,” “Jour. Amer. Med. Assoc.,” 1898, xxx, 217-219. 154. Purjesz, Sigmund, “Deutsches Arch. f. klin. Med.,” Bd. xxm, S. 554, 1879. 155. Quincke, “Dilation with Rupture into Colon,” “ Correspondenzbl. f. Schweizer Aerzte,” 1874. 156. Reed, B., “Dilation of the Stomach, with Reports of Cases Treated by Diet, Massage, and Intragastric Electricity,” “Jour. Amer. Med. Assoc.,” 1898, xxxi, 220-223. 157. Reed, W. W., “Report of a^Case, with Remarks upon the Diagnosis of Pyloric Stenosis,” “Colorado Med. Jour.,” Denver, 1898, iv, 139-144. 158. Reichmann und Heryng, “Ueber Gastrodiaphanie,” “Berl. klin. Wochenschr.,” 1892, Nr. 51. 159. Remond (de Metz), “ Gaz. des Hopit.,” 14 Nov., 1891. 160. Revilliod, “ Revue de Med. de la S. Romande,” No. 1, 1885. 161. Riegel, “ Zur Diagnose u. Behandlung der Magenerweiterung,” “ Deutsche med. Wochenschr.,” 1886, Nr. 37. 162. Riegel, “Ueber Diagnostik u. Therapie der Magenkrankheiten,” “ Volkmann’s klin. Vortrage,” Nr. 289. 163. Robson, A. W. Mayo, “ Tetany and Tetanoid Spasms Associated with Gastric Dilatation Treated Surgically,” “ Lancet,” Nov. 26, 1898. 164. Rosenbach, “ Berlin, klin. Wochenschr.,” Nr. 51, S. 742, 1876. 165. Rosenheim, “Ueber d. Verhaltn. d. Magenfunkt. nach Resekt. des carcinomat. Pylorus,” “Deutsche med. Wochenschr.,” 1892, Nr. 40. LITERATURE. 68 I 1 66. Rosenheim, F., “ Ueber motorische Insufificienz des Magens,” “ Berlin, klin. Wochenschr.,” 1897, xxiv, 228, 252 ; Discussion, 256. 167. Rosenthal, “ Magenneurosen und Magenkatarrh,” Wien, 1886, S. 181. 168. Rosenthal, A., “ Preliminary Note on Disorders of Mobility of the Stomach, Myasthenia, Atony, and Ectasia,” “Chicago Med. Recorder,” 1898, xv, 176. 169. Rossler, A., “ Ueber die Ausschaltung der Ernahrung durch den Magen bei Dilatatio ventriculi,” “Wien. klin. Wochenschr.,” 1893, Nr. 40. 170. Rousseau, G., “ De la dilatation d’estomac chez les nourrissons,” These de Paris, 25, xi, 1896. 1 7 1 . Rupstein, “ Archiv f. Anat. u. Physiol.,” 1874. 172. Rydygier, “ Zur Magendarmchirurgie,” “Wien. klin. Wochenschr.,” 1894, Nr. 10. 173. Saundby, “ Deutsche med. Wochenschr.,” Nr. 42, 1896. 174. Schliep, “ Deutsches Archiv f. klin. Med.,” Bd. xm, S. 445. 175. Schmidt, “Berlin, klin. Wochenschr.,” 1886, No. 33. 176. Schmidt-Monnard, “ Hour-glass Stomach,” “ Munch, med. Woch- enschr.,” 1893. 177. Schreiber, “Archiv f. Verdauungskrankh.,” Bd. 11, S. 423. 178. Schwyzer, T., “ A Case of Congenital Hypertrophy and Stenosis of the Pylorus,” “ N. Y. Med. Jour.,” 21, xi, 1897. 179. See, G., et A. Mathieu, “ Rev. de Med.,” 10 Mai et 18 Sept., 1884. 180. Senator, “Ueber einige neuere Arzneimittel,” “ Berl. klin. Woch- enschr.,” 1885, Nr. 1. 1 8 1 . Senator, “On Autointoxications, etc.,” “ Zeitschr. f. klin. Med.,” Bd. vii, 1884. 182. Sievers, R., “On tetanie vid dilatation of magsaken,” “ Finska lak. sallsk. handl.,” Helsingfors, 1898, XL, 18-39. 183. Sittmann, “ Miinch. med. Wochenschr.,” 1893, Nr. 29. 184. Stockton, C. G., “ Gastrectasis from Pyloric Spasm,” “ Internat. Clin.,” Phila., 1898, 8 S., 1, 126-128. 185. Stoker, “Hour-glass Contract. Stomach,” “Med. Press and Circ.,” March 3, 1869. 186. Talma, “ Indicat. z. Magenoperationen,” “Berl. klin. Wochenschr.,” 1895. 187. Tappeiner, “ Zeitschr. f. Biol.,” Bd. v, 471. 188. Thiebaut, These de Nancy, 1884. 189. Tilger, “ Traction Diverticulum of Pyloric Region, Caused by Disloca- tion of the Gall-bladder,” “Virchow’s Archiv,” Bd. cxxxm, Heft 2; the same author, “ Congenital Stenosis of the Pylorus ” (/. c.). 190. Traube-Kundrat, “ Handbuch d. Kinderkrankh.,” Bd. iv. 191. Traube, “ Gesammelte Abhandlungen,” 1871. 192. Thorowgood, “Lancet,” 17 Fev., 1872. 193. Wagner, “Berl. klin. Wochenschr.,” Nr. 16, S. 229, und Nr. 25, S. 361, 18 April und 20 Juni, 1881. 194. Wegele, “ Die diatet. u. medicament. Behand. d. Magendarmerkrank.,” Jena, 1896. 195. Weiss, H., “ Der Sanduhrmagen,” “ Mittheil. a. d. Grenzgeb. d. Med. u. Chir.,” Jena, 1897-8, 1, 393-398. 682 HEMORRHAGE FROM THE STOMACH. 196. Winternitz, “Deutsche Medicinalzeitung,” 1891, Nr. 38. 197. Winternitz und Baum, “Wien. med. Presse,” 1873, Nr. 17. 198. Zabludowski, “ Zur Massagetherapie,” “ Berl. klin. Wochenschr.,” 1886, Nr. 26 ff. u. 36. 199. v. Ziemssen, “ Ueber physik. Behandl. chron. Magendarmerkrankimg," Leipzig, 1888. CHAPTER VIII. HEMORRHAGE FROM THE STOMACH (GASTRORRHAGIA). This symptom as it occurs in consequence of gastric ulcer and carcinoma has already been described in the chapters devoted to these subjects. Hematemesis, or vomiting of blood, is not a syn- onymous term with gastric hemorrhage, for the vomited blood may have had its origin in the respiratory passages, and have been swallowed. It may have come from the esophagus or from the duodenum. Then, again, there may be undoubted gastric hemor- rhage without hematemesis. The cause of the gastric hemorrhage may be found in injurious influences coming from without, or developing within, the stomach. Etiology. — 1. Gastric Ulcer. — This is the most frequent cause of hemorrhage. Tuberculous, syphilitic, or typhoid ulcers of the stomach are extremely rare; and even in those cases that are reported they are seldom mentioned as causes of hemorrhage. Professor William Osier described a case of profuse gastric hemor- rhage to the author which was caused by a typhoid ulcer of the stomach occurring at the Johns Hopkins Hospital. Erosions of the stomach, as such, do not, in my experience, cause hemorrhage, but when they are digested out by hyperacidity or supersecretion, they may break into the walls of a blood-vessel ; then, however, we can no longer speak of an erosion : it has become a peptic ulcer. 2. Malignant Tumors of the Stomach. — Carcinoma and sarcoma. 3. Be7iig7i Tumors of the Stomach. — These are rare causes of hemorrhage. 4. Mecha7iical, Chemical , and Theri7iic Causes. — (a) Acting from without, such as direct traumatism, or injury to the abdomen; penetrating wounds of the abdomen affecting the stomach. ( b ) Acting from within: swallowed foreign bodies, such as fish-bones, ETIOLOGY OF GASTKORRH AGIA. 683 pins, etc. ( c ) Corrosive chemical poison, such as mineral acids and caustic alkalies; poisons swallowed by mistake or with suicidal intent, (d) Exceedingly hot substances. ( e ) The HC 1 itself in a state of hyperacidity or supersecretion may erode small blood- vessels in places where the circulation is abnormal, where there are blood extravasations, emboli, or thrombi. (/) Injury caused by the stomach-tube. 5. Disease of the Gastric Blood-vessels. — ( a ) Galliard found mil- iary aneurysms of the arteries of the stomach as a cause of fatal hemorrhage, (b) The gastric veins may be affected by varices, this condition being generally associated with chronic passive congestion of the stomach. Recently, Lancaster has reported a case of fatal gastric hemorrhage in a woman aged thirty-three years. At the autopsy varicose dilatation of several branches of the gastro-epiploic vein in the greater omentum and in the submucosa of the stomach were found. The largest ones of these varices showed a rupture as large as a pin (“ Miinchen.med. Wochenschr.,” 1896, Nr. 45). ( c ) Fatty atheromatous and amyloid degenera- tion of the gastric blood-vessels. No reliable autopsy reports could, however, be found in which gastric hemorrhage was due to amyloid degeneration of the blood-vessels. Gastric hemorrhage in phosphorus-poisoning is attributed to fatty degeneration of the arteries. 6 . Active congestion of the stomach usually is a result of intense acute inflammation, which inevitably brings on inflammatory altera- tions in the vessel walls. W. H. Welch assigns the so-called vicarious hemorrhages from the stomach to active congestion. As a result of a large experience in cases of gastric hemorrhage, the author can confirm that periodic gastric hemorrhages occur simulta- neously with the menstrual period. In amenorrhea one occasionally observes periodic gastric hemorrhages. Sometimes, when a young female is afflicted with a gastric ulcer, the hemorrhages may coincide with the menstrual terms. Whether such hemorrhages are “ vicari- ous ” or not is difficult to decide. This term means “ substitutive ,” and is applied to the assumption of functions of one organ by another. In our opinion gastric hemorrhage can hardly substi- tute the physiological process of menstruation. It has been assumed that suppressed hemorrhoidal hemorrhage and epistaxis may be substituted by a gastric hemorrhage — a very hypothetical suggestion. 7. Passive congestion of the stomach , resulting from some obstruc- 684 HEMORRHAGE FROM THE STOMACH. tion to the portal circulation. Such obstruction can occur (a) in the portal vein itself or in its branches within the liver, as in cir- rhosis of the liver, neoplasms, echinococcus-cysts pressing on the portal vein ; also in pylethrombosis, and cholecystitis. Obstruc- tion to the flow of bile, and consequent dilatation of the bile-ducts in the liver, and pigment deposits in melanemia may cause occlusion of the capillaries in a similar way. ( b ) The obstruction may occur from failure of compensation in valvular and other diseases of the heart. ( c ) In the pulmonary blood-vessels caused by emphysema, chronic pleurisy, and fibroid indurations of the lungs. During violent acts of vomiting gastric hemorrhage is occasionally ob- served, and may be explained by the venous congestion of the mucous membrane of the stomach. Such hemorrhages have been observed by the author during vomiting of pregnancy and sea- sickness. The veins in the muscular layer of the stomach are much more likely to be compressed during the violent contractions of the gastric muscularis than are the arteries. Obstruction to the pulmonary or cardiac circulation is not so frequent a cause of gas- tric hemorrhage as obstruction in the portal vein or the liver. Next to ulcer and cancer of the stomach, cirrhosis of the liver is the most frequent cause of gastric hemorrhage. 8. Acute Infectious Diseases . — The manner and process by which gastric hemorrhage is brought about in these diseases are not well understood. It is usually explained by the dissolution of the blood-corpuscles and alterations in the walls of the blood-vessels. In a few instances only was the hemorrhage found to be due to plugging of the vessels with bacteria. The gastrorrhagia in acute yellow atrophy of the liver has been attributed to the simultaneous action of a variety of causes — for instance, dissolution of the blood by bacteria or bile constituents, together with obstruction of portal circulation due to disease and occlusion of the hepatic capillaries. The infectious diseases that are generally assigned as causes of gastric hemorrhage are yellow fever, acute yellow atrophy of the liver, malaria, relapsing fever, cholera, typhoid fever, typhus fever, erysipelas, diphtheria, small-pox, measles, and scarlet fever. g. Certain Constitutional Affections. — ( a ) Scorbutus, purpura, hematophilia, and other affections inducing a hemorrhagic diathe- sis. ( b ) Various forms of anemias ; progressive pernicious anemia, chlorosis, leukocythemia, and pseudoleukocythemia. (< c ) Malaria. The author has lived in the malarious regions of Virginia and Maryland along the Chesapeake Bay, and can assert from exten- NEPHRITIS — M ELENA. 685 sive experience that this disease is capable of causing hemorrhage from the stomach. Not only are the hemorrhages cured by quinin, but the malarial organism has been found by the writer in the vomited blood. Hans Herz in his new contribution, “ Die Stor- ungen des Verdauungsapparates als Ursache und Folge anderer Erkrankungen,” admits the influence of malaria in bringing about these gastric affections. We may distinguish (1) the periodical malarial gastric hemorrhage (curable by quinin); (2) the pernicious malarial gastric fever ; (3) gastric hemorrhages due to extreme anemia brought about by malarial cachexia; (4) cholemia. This is attributed to dissolution of the blood-corpuscles by biliary con- stituents. 10. Nephritis . — In very rare instances hemorrhage from the stomach has been reported in connection with contracted kidneys. Wm. H. Welch found the cause of a fatal gastric hemorrhage in one such case to be due to the bursting of a miliary aneurysm of a smalt artery in the submucous coat, and he considers that all similar hemorrhages occurring in such cases are referable to disease of the vessel walls (Pepper’s “ System of Medicine,” vol. 11, P . 582). 11. Melcena Neonatorum . — An extravasation of blood into the stomach and intestines of the new-born infant, occurring most often in the first few hours of life. Large quantities of blood are lost by the intestinal evacuations or by vomiting. The origin of this disease is very obscure. In some cases it seems to be an infection ; in others, scorbutus or hemophilia seems to lie at the foundation. In rare cases gastric and duodenal ulcers have been found. Landau (“ Ueber Malaena, Habilitationschrift,” Breslau, 1875) and others have ascribed it to embolism of the umbilical veins. They presume that thrombi become detached from this vein and the ductus arteriosis, and reach the gastric or intestinal arteries. W. Soltau Fenwick (“ Disorders of Digestion in Infancy and Childhood ”) reports a case in which postmortem examination failed to explain the origin of the bleeding, but when the vessels of the stomach were subsequently injected, a large vein was dis- covered close to the cardiac orifice, through an aperture in which the injection poured out in great quantities. Fenwick correctly suggests that in many cases the cause of the bleeding is not detected because postmortem contraction of the mucous mem- brane may have obliterated the signs of rupture of some varicose vein in the stomach or bowel. Among twenty cases recorded by 686 HEMORRHAGE FROM THE STOMACH. Rilliet and Barthez (“ Trait, des Malad. de l’enfance,” 2d edition, vol. ii, pp. 295-310), nine exhibited melena within thirty-six hours, and seventeen before the sixth day. Silbermann (“ Gerhardt’s Handbuch,” iv, S. 415) reported thirty-seven cases, in twenty-seven of which the hemorrhage occurred within the first two days. The clinical picture of this fatal infantile disease is, in brief, about as follows : The child is very anemic, the evacuations consist of thick, dark blood, and are followed by collapse or great restlessness. The stools succeed one another in rapid succession, and soon consist entirely of bright blood. The hemorrhage from the bowels con- tinues for about twenty-four hours ; hematemesis is not so fre- quent. If the loss of blood is excessive, the infant succumbs to heart failure; but even in the less severe cases, in which it gradu- ally improves, it will remain anemic for many weeks, or eventually die of some acute gastrointestinal disease. The mortality of melena is variously stated at from sixty to seventy-five per cent. E. von Preuschen (“ Centralbl. f. Gynakol.,” xviii, 9, 1894) bases his explanation on the fact that blood extravasations were found in the brains of the infants simultaneously with melena. Accord- ingly, he regards the brain lesion as the cause of the disease. Suffice it to say that frequently no blood extravasation has been found in the brain in these cases, and that it may also rationally be interpreted as the contemporaneous expression of the same severe constitutional disturbances. F. Gartner (“ Archiv f. Gynakol.,” xlv, 1893) claims to have discovered the cause of an infectious dis- ease in infants analogous to melena. In fact, he calls this organism the bacillus of melena. His researches have, as yet, not been con- firmed. Grynfelti (“Arch, de Tocol. et Gynecol.,” Bd. xix. Nr. 6) compares melena to the disencumbering discharge of blood occur- ring through the hemorrhoidal veins in chronic diseases of the liver. It is not impossible that the sudden closure of the um- bilical artery may cause a collateral overfilling of the other abdom- inal organs. L. Fischer (“ Munch, med. Wochenschr.,” xliv, 1897) suggests that such an excess of blood may be caused by a late ligation of the umbilical cord, but all of these explanations, although very interesting, are conjectural. 12. Nej'vous Conditions . — The experiments of Schiff, Brown- Sequard, Ebstein, and Ewald make it probable that injury to the cerebral peduncles — optic thalami, corpus striatum, the crura, and the anterior corpora quadrigemina — may cause gastric hemor- rhages and formation of peptic ulcers. This is a justifiable deduc- I D I OPAT H I C HEMORRHAGE. 687 tion when we are dealing with physiological experiments, but there is no evidence that gastric hemorrhage sufficient to be of clinical im- portance can be caused by lesions of the central nervous system. A number of the most conservative authors hold that gastric hem- orrhages occur in hysterical women. Personally, I have had no opportunity to observe an unmistakable case of hemorrhage from the stomach in a hysterical woman that could not be explained in some other way. I do not wish to deny that it occurs, but the chance of deception by crafty patients is great. It should be men- tioned in this connection, that in patients suffering from undoubted gastric ulcers hemorrhages are liable to occur after psychical and emotional excitement. Hemorrhages from the stomach, which have been reported to occur in locomotor ataxia, in tubercular meningitis, in epilepsy, and in progressive paralysis of the insane, may be classified under this heading, but are largely attributable to other causes. ij. The Rupture of Abscesses or of Aneurysms from Adjacent Organs into the Stomach. i/f. Idiopathic Gastric Hemorrhage. — Wm.H. Welch (/. c.) assigns a place to hemorrhage attributed to this cause, quoting from Flint (“ Principles and Practice of Medicine,” 5th edition, p. 513); “ Hemorrhage sometimes occurs from the stomach, as from the bronchial tubes, the Schneiderian membrane, and in other situations, without any apparent pathological connections, neither following nor preceding any appreciable morbid conditions. It is then to be considered as idiopathic.” Apparently healthy persons, it is claimed, suddenly have profuse gastric hemorrhages, which are followed only by symptoms immediately referable to the bleeding. They develop no further symptoms, and often have no other hemorrhage. Personally, we consider that so-called idiopathic causes should have no place in the etiology of gastric hemorrhage. The sources of error are too great to be eliminated by a microscopic examina- tion of the stomach. We have already referred to the cases of Lancaster and Soltau Fenwick of fatal hemorrhages resulting from pin-point openings in gastric vessels. Orth and Chiari have reported similar cases. Capillary hemorrhages can very often not be demonstrated at all. One must not overlook the fact that hem- orrhage from the stomach is not the only cause of hematemesis. The source of the blood, which may have gained access to the stomach, may be in the mouth, nose, throat, bronchial tubes, 688 HEMORRHAGE FROM THE STOMACH. esophagus, or the duodenum. Ewald (“ Real-Encyklopadie,” 3. Aufl., xiv, “ Magenkrankheiten,” p. 288) reports a case of fatal gastric hemorrhage with absolutely no lesion in the stomach or anywhere in the digestive tract. A. Frankel (“ Deutsch. Med. Wochenschr.,” 1894) reported a case of fatal gastric hemorrhage in an anemic patient due to slight capillary erosions. Pathology. — It can not be considered the object of this work to describe the manifold lesions that are found after death from gastric hemorrhage. It is sometimes very difficult to find the source of fatal gastric hemorrhage. Often it has proved fruitless. In such cases writers have overcome the difficulty by assigning the cause of the hemorrhage to diapedesis, and not to rupture of a blood-vessel. In most cases of gastrorrhagia the outpouring of blood is very sud- den and profuse, and the conception of diapedesis does not justify the belief that the red corpuscles can escape through the unrup- tured walls of blood-vessels with that combined rapidity and abundance that is necessary to explain the typical gastric hemor- rhage (Welch, /. c.). In Welch’s case of bursting of a miliary aneurysm, over an hour of continuous searching was required to find the pin-hole perforation in the bottom of which lay the small aneurysm. The erosion in Chiari’s case (“ Prag. med. Wochenschr.,” 82, Nr. 50) was not larger than a hemp-seed. The more pains- taking and careful the search after the source of the hemorrhage is made, the more frequently will a definite anatomical lesion be found as the cause. Injection of the gastric vessels with some highly colored fluid aids in finding the ruptured vessel. Symptomatology. — There are cases of undoubted gastric hemorrhage that present no symptoms whatever. Very small amounts of blood do not lead to vomiting, and are not sufficient to produce visible alterations in the stools. As a rule, patients do not observe the character of their stools. Very frequently the stools are not even observed by the attending physician. It fol- lows that it is possible for large gastric hemorrhages to escape detection when the blood escapes exclusively by way of the intes- tines. In cases of sudden pallor and weakness, as occur in patients suffering from gastric diseases, and even in such as have hitherto presented no history of gastric disease, the stools should by all means be examined. The symptoms that lead up to gastric hemorrhage are described in the chapters on Ulcer and Carci- noma. The symptoms that are directly brought about by the loss of blood are, in severe cases, fainting, unconsciousness, and con- SYMPTOMATOLOGY OF GASTKORKH AGIA. 689 vulsion ; but when the hemorrhage has not been profuse, the patient feels a progressive weakness and languor. Sometimes a giddiness, vertigo, tinnitus, and flashes before the eyes are com- plained of. In copious bleeding, nausea and vomiting are, as a rule, produced; but whether the bleeding was copious or not, the symptoms of anemia sooner or later become evident. The appear- ance of the vomited blood will vary according to the time it has remained in the stomach prior to emesis, according to the source of the hemorrhage, — that is, whether it be arterial or venous, — and the condition of the gastric juice, and whether remnants of food were in the stomach at the time the rupture of the vessel occurred. Food that has remained in the stomach for a longer time assumes a dark brown or chocolate color or the appearance of coffee-grounds under the action of the gastric juice. The quantity may vary from thirty grams to one liter or more. It is sometimes difficult to estimate the total quantity of blood that has been lost, because a certain portion of the blood is invariably lost by the stools. In certain cases the entire quantity of blood lost by rup- ture of a gastric blood-vessel passes into the intestines; larger admixtures of blood to the stool can be easily recognized when the administration of iron or of bismuth can be excluded. Smaller quantities can not be recognized by inspection. In this case some of the tests described in chapter xm will have to be gone through. Although a hemorrhage has been very copious, it may be re- peated several times — at short intervals. Rise of Temperature After Gastric Hemorrhage . — After a copious loss of blood, rise of temperature can be experimentally produced in animals. This fever, which has been termed anemic fever, is not peculiar to gastric hemorrhages, but occurs in a similar manner from hemorrhages from other organs. It was first emphasized by Leichtenstern that a mild or a high fever is a frequent and even regular phenomena of gastric hemorrhage caused by peptic ulcer. This does not signify that fever indicates that the hemorrhage has come from an ulcer; it is frequently observed in hemorrhages from carcinoma, and even from the hemorrhage resulting from passive congestion in certain forms of chronic gastritis. It is quite well known that fever usually follows venesection. The term anemic fever merely suggests that it occurs with various hemorrhages leading to anemia. The intensity of the febrile reaction is largely influenced by two factors — viz., the rapidity and the quantity of the 690 HEMORRHAGE FROM THE STOMACH. hemorrhage. Small hemorrhages are, as a rule, not followed by elevation of temperature. The pathological physiology of this fever is very obscure. In advanced anemia the blood stagnates in the internal organs, while the peripheral parts become deficient in blood and cooler, and the rate of the blood-current is considerably reduced; thus the loss of heat from the surface is diminished, and the heat of the internal parts is increased. In the author’s opinion this is the most probable explanation. Other theories explain the fever by an invasion of bacteria through the ruptured blood-vessel ; by the resorption of putrefying blood-masses from the intestine; and by the assumption that advanced anemia stimulates the heat centers in the medulla. This fever may last several days, and is accompanied by marked acceleration of the pulse. The rate of the beat can frequently be determined only by auscultation over the heart, the radial pulse being frequently imperceptible. Notwithstanding this, the impulse of the apex-beat may appear intensified. The Disturbances of Sight — Blindness After Gastric Hemorrhages. — These are extraordinary and rare complications of copious loss of blood from the stomach, and are known to occur after hemor- rhages from other organs. But although hemorrhages from other organs are frequent, disturbances of sight, as a consequence, occur only exceptionally. It has been argued that in uterine hemor- rhages the slowness of the effusion, and in traumatic hemorrhages the otherwise healthy condition of the patient, prevents a develop- ment of eye phenomena. It is well known that copious hemor- rhages from the lungs in phthisical patients are not followed by optic phenomena. Blindness has, however, been observed after very violent attacks of vomiting unaccompanied by any evidence of hemorrhage, which suggests that perhaps the act of emesis may be instrumental in the production of these eye symptoms. These disturbances of sight may occur immediately after the hemorrhage, but, as a rule, they do not appear until from the fifth to the eighth day, but they have been observed as late as the twenty-fourth day. Slight attacks of amaurosis, amblyopia, or even transient blindness, are sometimes overlooked because other graver symptoms step to the foreground, and when the strength of the patient is very much spared, owing to extreme prostration, there is little opportunity for using and testing the eyesight. Fortunately, the disturbances of sight disappear in the majority of cases, but in others permanent blindness of one or both eyes may result. The § DIAGNOSIS OF GASTKOKKH AGI A. 69 usual result is recovery with a slight defect of sight, such as irreg- ularities in the visual field, color-blindness, etc. Forster has observed extravasations in the retina and grayish clouding around the papilla immediately after the hemorrhage. In some cases these changes did not produce any symptoms whatever in other cases they led to atrophy of the optic nerve. According to Knies, ophthalmoscopical examination is often entirely negative ; at other times he found merely a pale papilla and very narrow blood-ves- sels, and finally complete atrophy of the optic nerve such as occurs in retrobulbar neuritis. In a few cases he claims to have observed complete choked disc, and finally in a number of cases an entirely normal fundus and papilla. The cause of the eye affection is not known. Gowers attributes it to an influence in the nature of shock on the nerve elements of the retina. Forster supposed that malnutrition of the nerve-fibers, swelling, and clouding occurred through absorption of water from the vitreous substance. Ziegler demonstrated fatty degeneration in the optic nerve and retina, particularly in the neighborhood of the lamina cribrosa; results which he attributes to ischemia. Ulrich assumes a circulatory disturbance at the edges of the papilla where the retinal vessels are bent in a sharp angle; this compels the intraocular pressure to remain unchanged, while the general blood pressure rapidly sinks. Knies locates the changes in the optic nerve itself, not in the retina. There are disturbances of sight after gastric hemorrhages which appear to be of cerebral origin. They are usually not permanent, but clinically they are distinguishable from those previously de- scribed. The reaction of the pupil is preserved ; there may be total blindness, or hemianopia. Diagnosis. — In all cases of hematemesis it will be necessary first to decide whether the material vomited is really blood, because a color more or less resembling that of altered blood may be pro- duced in the vomit by iron, bismuth, claret, fruits, — such as black- berries, mulberries, cranberries, — and bile. One or other of the tests for blood in the stomach-contents given in chapter xm will here become necessary. We recommend the modification of Van Deen’s method, suggested by H. Weber. And, secondly, it must be ascertained whether the blood is really from the stomach, and not from the nose, throat, or the esophagus. Here a careful ex- amination of the respiratory passages, of the mouth and nose, will generally reveal the source of the bleeding. The differential diag- 692 HEMORRHAGE FROM THE STOMACH. nosis between hematemesis and hemoptysis is given in the chapter on Gastric Ulcer. In doubtful cases the microscope may reveal tubercle bacilli in case the hemorrhage came from the lungs. The differential diagnosis between these two causative conditions presents difficulties when there are indications of pulmonary tuberculosis simultaneously with those of gastric ulcer. Hemor- rhages that come from the esophagus, especially the lower portion of it, can hardly be distinguished from genuine gastric hemor- rhages. Several cases have been reported of fatal hemorrhage from varices of the esophagus, and the esophagoscope has been suggested as a means for differential diagnosis. In recent hem- orrhages from the stomach and esophagus, however, the use of so rigid and annoying an instrument to the patient as the eso- phagoscope is unjustifiable. A microscopic examination of vomited matter may often reveal intact red blood-corpuscles, making the diagnosis definite. It has been suggested that in hemorrhages from the esophagus the blood, as a rule, is not mixed with food remnants; but in stenosis of the esophagus the ingesta accumu- lates above the constriction, and may therefore be vomited up mixed with blood; but the food in esophageal vomiting is alkaline, undigested, mixed with mucus, saliva, and perhaps blood ; food brought up from the stomach is more or less digested, has an acid reaction, and contains products of peptic digestion. Vom- iting of blood occurs in about fifty per cent, of all cases of gastric ulcer. The next most frequent cause is carcinoma. But there is a variety of other abnormal conditions of the stomach which may bring forth this symptom ; these are : (1) Acute and chronic gastritis. Teissier reported a case of an alcoholic subject suffering from chronic gastritis who showed frequent vomiting of food and blood. The autopsy showed a simple chronic inflammation of the stomach with hypertrophy. (2) The gastric hemorrhages occur- ring periodically and associated with abnormal conditions in other organs. We have considered these possibilities in the etiology. DaCosta mentions vicarious gastric hemorrhage in patients suffer- ing from hemorrhoids. The author has never seen a case of this sort. The gastric hemorrhages that occur from ischemia due to per- sistent vomiting are at times puzzling. During a voyage to Bremen in 1896, the author had occasion to study a case of this kind. A healthy young man, age twenty-two, suffered intensely from seasickness. For the first three days he vomited every- thing he ate, and when his stomach was empty, the nausea would HEMATEMESIS NOT DUE TO ULCER. 693 continue, although nothing but a little mucus was forced up, under painful exertions. On the seventh day of the voyage he vomited half a liter of blood, and on the eighth day about ^ of a liter. After that he was, by the author’s suggestion, kept constantly under narcotics. The hypodermic injections of morphin proved most effective in allaying the vomiting, ice-bags were placed over the epigastrium, and the patient’s strength kept up by nourishing enemata. Although he vomited blood on three other occasions after that, the amount was small. After our arrival in Bremen he recovered entirely, and could eat almost the regular hotel menu. This patient had never previous to this voyage suffered from any gastric disease, and his vomiting of blood could be attributed only to the persistent emesis caused by the sea-sickness. I have observed a number of cases similar to this in hospital and consultation practice where hematemesis was brought on by uncontrollable vomiting of pregnancy. One case of death from vomiting in pregnancy, in which one pint of blood was vomited the day before the fatal termination, the stomach showed numerous hemorrhagic infarcts. Extravasations of blood had occurred in the submucosa, and under the columnar epithelium, lifting it from the glandular layer. The death of this patient was due to ex- haustion, because not even rectal enemata could be retained, and operative evacuation of the uterine cavity had been refused. In chlorotic and anemic patients that present hematemesis it is wise to be reserved in the diagnosis of gastric ulcer. In all such cases a careful blood-count should be made, and a prolonged course of iron and arsenic undertaken before the diagnosis of gastric ulcer should be determined upon. The diet of such cases should be that of ulcer. The following is an example of how puzzling cases of gastric hemorrhage may be clinically : A male patient in the author’s private sanatorium had been complaining for two years of intense gastric pains, which recently had become so aggravated as to cause refusal of food, and consequent rapid emaciation. The test-meals showed a slight excess of free HC1, equal, on the average, to 38 degrees, normal NaOH. One morning, while the patient was being examined by the author, he began to vomit his breakfast, and after the food had all been evacuated, about one pint of pure blood was vomited. The pain in the epigastrium was somewhat more severe for several days after this attack, and on this account an exploratory laparotomy was advised. At the operation, which 46 694 HEMORRHAGE FROM THE STOMACH. was done by Dr. J. M. T. Finney, the stomach was found entirely normal, it was not enlarged, presented no abnormalities of any kind. There were a number of enlarged mesentery glands, one of which was excised by the surgeon, but on histological examina- tion it showed nothing characteristic. The patient recovered from the laparotomy, and under a very carefully selected diet and use of external heat to the epigastrium with rest in bed the pain was cured. He was kept under observation for six weeks, and dis- charged apparently cured. Three months after the operation he was reported as doing very well. Prognosis. — We do not wish to refer here to the prognosis of the fundamental disease causing the hematemesis, which is spoken of in other chapters, but merely of the hemorrhage itself. This prognosis depends upon the quantity of the blood lost. The most abundant hemorrhages are observed in gastric ulcer, but even larger hemorrhages, are, as a rule, not dangerous to life. We have repeatedly observed recovery from gastric hemorrhage that had led to collapse with disappearance of the radial pulse. The dan- ger of gastric hemorrhage exists in an early and rapid repetition of the loss of blood ; though we have seen one case of profuse gastric hemorrhage which led to death in[a very short time — we should conjecture about fifteen minutes. Treatment. — The treatment of this symptom has been given under the heading of Gastric Ulcer. Here we wish to repeat once more the necessity of absolute rest, of moral encouragement from the physician, — assuring his patient that the symptom is entirely free from danger, and will be recovered from, — total abstention from any food or medicine by the stomach, and substitution of rectal feeding. Internal medication during the bleeding is danger- ous. The author favors a hypodermic injection of ergotin or ergotol, of the latter thirty minims. Whenever there is danger of collapse from very profuse loss of blood, subcutaneous or intra- venous injection of normal salt solution is strongly recommended. A solution of 0.6 to 0.75 per cent, of sodium chlorid is used for this purpose. We prefer the subcutaneous injection to the intra- venous, because it requires less apparatus, is rapidly executed, and free from danger. About 200 c.c. of this salt solution may be in- jected into the subcutaneous connective tissue of the breast in this manner, and with the aid of massage it is generally rapidly absorbed. The subsequent treatment is that of simple anemia and of the causative condition. HISTORY AND PATHOGENESIS OF ENTEROPTOSIS. 695 CHAPTER IX. ENTEROPTOSIS— GASTROPTOSIS. CONCERNING THE HISTORY AND PATHOGENESIS OF ENTERO- PTOSIS. The term enteroptosis comes from the two Greek words, tvTepov, bowel or intestine, and nruxTiq, fall. It refers to a dislocation of the abdominal organs. Splanchnoptosis is a synonymous term. Entero- ptosis is a disease in which the liver and the kidneys have descended from their normal positions, and are movable. The stomach is often found descended and to have assumed a vertical position, which induces an atony of the gastric wall with motor and secre- tory disturbances. The transverse colon, particularly the hepatic side of it, is found descended. Generally only one kidney, the right, is dislocated or very movable. The terms hepatoptosis, nephro- ptosis, gastroptosis, and coloptosis refer to the particular organ which has become displaced. The oldest description resembling such a clinical picture is found in Aberle’s work (/. c .) ; and similar instructive anatomical accounts are found in the works of Becquet, Rollet, Rayer, Oppolzer, and Chrobak, referring to the relation between hysteria and movable kidney. The causes as- signed by these various older writers to the production of movable kidney are manifold, and some of them are even at the present time still considered factors in the etiology of enteroptosis; one of the earliest explanations is contusion of the renal region. Various other traumatisms are accused of bringing about this effect ; par- ticularly severe coughing attacks, such as occur in pertussis, bronchitis, and pleurisy, which exert their pernicious effect espe- cially when rapid emaciation has occurred, as in phthisis, producing disappearance of the fat in the adipose capsule surrounding the kidney; or when a pleuritic exudate brings about descent of the diaphragm, and thereby of the liver and kidney. In the opinion of Cruveilhier, Chapotot, and Valker the corset is an important cause in the development of this disease, and although Ebstein denied this, Weisker and Meinert have recently sup- ported this explanation. Becquet considers that the floating kidney is intimately connected with the sexual life of woman, and explains it by the congestion of the kidneys which occurs 696 ENTEROPTOSIS GASTROPTOSIS. during menstruation, as a result of the intimate connection be- tween the ovarian and renal plexus. He also associates the trouble with frequent births, uterine diseases, and pendulous abdomen. I have seen a liver in an autopsy on a young woman, age twenty- four, who died from intestinal perforation in typhoid fever, which showed very marked grooves evidently produced by tight lacing. The transverse colon, stomach, and the right kidney were dis- placed, and the lower portion of the thorax compressed in a funnel- shaped manner. Opolzer believes that rapid emaciation in wasting diseases is a cause. Dietl has observed movable kidney in four cases after severe malarial and typhoid fever. He believes that in these infectious diseases marked change in volume in the abdominal organs occurs. Rollet argues in favor pf rapid emaciation, and adds the pressure created by large neighboring organs, especially hepatic and splenic tumors. He suggests the possibility of inherited pre- disposition. In experiments on cadavers Heller could not confirm the view that traction made upon the kidneys by dislocations of the female sexual organs could effect renal displacement. In 1881 Landau published a very complete monograph on float- ing kidney. In explaining the etiology of the disease he empha- sized three factors: (1) Rapid disappearance of the fat in the adi- pose embedding of the kidney, and laxity of the peritoneum. The disappearance of the fat must be rapid, because Landau considered it possible that an accommodation might be effected through the elasticity of the capsule. (2) Disease of the abdominal walls, which are subjected to considerable changes in their elasticity, density, and resistance by pregnancy and abdominal tumors. In rapidly consecutive pregnancies the condition known as pendulous abdomen may be developed. Normally, there is a uniform pres- sure on all abdominal organs, but in cases of pendulous abdomen this is converted into the opposite condition, and the intestines that hang into the relaxed abdominal bag exert a traction upon the super- imposed organs. (3) The numerous displacements of the genito- urinary organs, which exert a direct traction, upon the kidneys by way of the ureters. Among forty-two observations by Landau, only two were nulli- parae, and one of these had been operated on for an ovarian tumor. Litten was the first to distinguish between congenital and ac- quired dislocation of the kidney, and also between dislocated kidney with and without movability. His differentiation between OBSERVATIONS ON GASTROPTOSIS. 697 a movable kidney and a floating kidney that has developed its own mesentery is a masterpiece of clinical diagnosis, containing also a description of the possibilities of respiratory movements that are imparted to the right kidney, particularly by the diaphragm and the liver, thus explaining the predisposition of the right kidney to abnormal movability. Kuttner argues that a kidney that has become loose in its adipose capsule follows the movements of the diaphragm in a more extensive manner. He explains the more frequent movability of the right kidney by assuming that the upper end of this organ gradually glides under the lower surface of the liver, and is thereafter completely dislocated by the hepatic pres- sure to which the respiratory movements are superadded. James Israel first observed the respiratory movements of the kidney during an operation in which the lumbar regions had been opened. Bartels observed dilation of the stomach together with movable kidney, and was one of the first to describe the simultaneous dis- location of several abdominal organs. This author and his pupil, Muller-Warneck, advance a theory explaining the production of dilation of the stomach by a floating kidney : — the right kidney, which has become dislocated, according to their conception, presses on the descending portion of the duodenum, which is firmly attached to the posterior abdominal wall by the peritoneum. The exit of the gastric chyme is prevented by compression of the duodenum, and gastrectasia is the consequence. OBSERVATIONS ON GASTROPTOSIS. J. E. Meckel first observed in autopsies the so-called vertical position of the stomach, and also that this occurred more fre- quently in females, but occasionally also in men. Kussmaul gave the first clinical description of the vertical position of the stomach, of which he distinguished two kinds, — the first was congenital, and represented an arrest at a fetal stage of development, and the second was acquired, caused by the pressure of lacing. The movable pyloric portion of the stomach is forced downward and toward the left by the descending liver, and the cardia is held in its position near the median line. Kussmaul observed that a stomach of normal size which had been forced into vertical position became displaced beneath the umbilicus. This occurs when the pylorus is moved to the left nearer the spinal column while the cardiac portion with the fundus is moved to the right and down- ENTEROPTOSIS — GASTROPTOSIS. ward. When the cardia and pylorus are approximated in this manner, the lesser curvature is converted into an acute angle. The descending arm of this angle becomes shorter and shorter, while the ascending arm becomes longer, the stomach thereby assuming the form of an intestinal loop, and gradually sinking below the umbilical line. (See illustration in chapter on Motor Insufficiency.) In one of the cases described by Kussmaul the wearing of the corset was blamed for the production of the con- dition, because of very evident and deep furrows on the lower thorax which were undoubtedly due to lacing. A similar view is held by von Ziemssen, who credits the so-called vertical position of the stomach as being productive of many ail- ments, and occurring principally in women. He believes the con- dition is most generally acquired during youth by excessive con- striction of the waist in lacing. As a consequence of this, the stomach can only escape in a downward direction, because the lacing compresses the region of the lower ribs, and the epigas- trium offers no space when the stomach is filled with food. The pyloric part, which is the most movable, makes the most extensive excursions, and gradually assumes the lowest position. At the same time, the duodenum is drawn down under strong tension of the hepatoduodenal ligament. According to Meinert, the normal position of the stomach in the female sex is the exception. Ac- cording to him, gastroptosis is a drawing out of the pyloric portion mainly — connected with dislocation. He does not think that it usually involves the entire stomach, and seeks its cause in patho- logical changes of the liver, or in the pyloric portion of the stomach itself. The most frequent cause, according to Meinert, is a patho- logical change of form of the thorax. When these deformities of the thorax and their causes — such as pressure caused by cloth- ing, or peculiarities of profession, and rachitis — have influenced a series of generations, they are, in Meinert’s opinion, capable of being transplanted by inheritance upon both sexes. They are then not congenital, but developmental, abnormalities. Historical Observations on Dislocation of the Colon. — We shall presently refer to Virchow’s contribution to our knowl- edge of coloptosis, to which he concedes great importance as a primary factor in the dislocation of the abdominal organs. He asserts that abnormal flexures occur in the majority of adults, the most frequent abnormality being a descent of the transverse colon, HISTORY OF COLON AND LIVER DISLOCATIONS. 699 the next most frequent being a descent of the hepatic flexure, and, lastly, of the splenic flexure. The simultaneous existence of floating kidney and dislocated colon is described in the autopsy protocols of Sandifort and Aberle. Leichtenstern describes ab- normal position of the colon, and attributes it to abnormal conditions of growth and position dating from the fetal period. He also suggests that a defective development of the muscular ligaments of the colon and incomplete descent of the cecum, also abnormally developed colon, and abnormal length of the mesen- teries, are possible causes. Rosenheim holds very similar views. Landau describes the descent of the hepatic and splenic flexures of the colon as quite constant accompaniments of floating kidney. Historical Observations on Dislocation of the Liver. — The liver may become displaced in two manners — (i) temporarily, by pressure from above, such as is caused by lacing or by pleural effusions; (2) permanent displacement, caused by disease of the liver itself, increasing the volume of the organ, and causing descent by its augmented weight. The oldest article on dislocation of the liver is by Cantani, published in 1866. There is much diversity of opinion as to the frequency of dislocated liver. Meisner thinks the hepatic dislocation is caused by lengthening of the suspensory ligament of the liver, forming a peritoneal fold analogous to that attached to the right hepatic lobe in many animals, and known as the “ mesohepar.” The direct cause of the dislocation he finds in traumatism. According to Winkler, the stretching of the ligament is passive and secondary; the first cause, in his opinion, being the sinking of intra-abdominal pressure. The other causes, which are accentuated repeatedly, are relaxation of the abdominal walls, physical overexertion, repeated overexertion of the abdominal muscles, and rapid emaciation. L. Landau holds that the fixation of the liver is effected through pressure of the abdominal muscles on the viscera and by the elasticity of the lungs, which arch up the diaphragm. The so-called ligaments of the liver are insufficient to retain the organ in position. The only anatomical attachment of importance is that of the liver to the inferior vena cava, by means of the hepatic vein. This attachment explains why descent of the organ as a whole does not occur more frequently than do partial dislocations of the anterior margin or of the right lobe ; under such conditions a partial rotation of the liver around its frontal or sagittal axis occurs. To this condition Landau has given the name of “ twisted,” 700 ENTEROPTOSIS GASTROPTOSIS. “ rotated,” or “ torsion, liver.” He has observed it almost always in connection with floating kidney and descent of the transverse colon, a combination practically identical with the clinical picture of en- teroptosis. Historical Views on General Enteroptosis. — These were the views held concerning the etiology of the dislocations of the vari- ous abdominal organs when Glenard’s first publication appeared in 1885. The writings of Ewald and Meinert, which have already been quoted, were published after those of Glenard. The ideas of the latter are dwelt upon in another portion of this article. For the sake of context, it may be repeated that a descent of the right or hepatic flexure of the colon, followed by dislocation of the trans- verse colon, is the primary disturbance in enteroptosis, according to this author. That portion of the mesocolon that approaches the right flexure of the colon he calls the hepatocolic ligament, and con- siders that it is naturally very weak, and can be loosened and stretched by the weight of the transverse colon, particularly when this is burdened with stagnating feces. The same condition may, according to him, also be caused by exhausting and emaciating dis- eases, by loss of tonicity of the abdominal muscles, by repeated pregnancies, by gastrointestinal autointoxication, by exhausting hemorrhage, or when the abdominal muscles are permanently dam- aged by pressure of the clothing. When the hepatic flexure of the colon has sunk, the right half of the transverse colon follows, up to the place where it is connected with the pyloric end of the stomach by the tense gastrocolic ligament ; here the colon becomes kinked, whereby stagnation of the contents results. The colon becomes dilated in front of the constriction, but beyond this it contracts so that it can be felt as a tense cord. After the transverse colon has descended, the remaining abdominal viscera follow as their ligaments become loosened. The stomach is drawn down by the traction on the gastrocolic ligament. Then follow the liver and the kidneys. Ewald has confirmed the observations of Glenard, but he did not confirm his views regarding the primary factor in the causation of the splanchnoptosis. The contracted portion of the colon beyond the constriction, which Glenard had designated as the “ corde colique transverse,” is considered by Ewald to be the pancreas. He also denies that a simple kinking of the colon, uncomplicated by peritonitic adhesions or by stenosing neoplasms, can lead to stag- nation of feces. Similarly to authors previously quoted, Ewald does PATHOGENESIS OF ENTEROPTOSIS. 701 not assign a distinct cause for this visceral anomaly, simply empha- sizing the fact that long-standing dyspepsias and bodily overexer- tions may create altered relations of pressure and tension, and thereby lead to enteroptosis. Ebstein, Litten, and Rollet inclined to the view that floating kidney was a congenital abnormality. They based their conclusions on the presence of a mesonephron. The vertical position and descent of the stomach was considered by Kussmaul a congenital abnormality, and Leichtenstern held the same view regarding dis- placement of the colon. Drummond held the opinion that a congenital relaxation of the peritoneal covering was the condition under which the kidney became movable. Ewald, Lindner, and Kuttner, — comparatively recent writers on the subject, — realizing that all explanations made hitherto were more or less hypothet- ical, have inclined also to the theory of inherited predisposition ; but Landau considers a cbngenital predisposition improbable. Although partial dislocations of individual viscera, and even of two or three of these organs at the same time, have been observed and described by other authors quoted, the first com- plete clinical representation must be credited to Glenard. But one can not fail to be impressed with the fact that the explana- tions of the etiology given by Glenard himself, as well as by writers antedating and succeeding him, are widely divergent. It is appar- ent from the writings of these authors that the order of displace- ment and the new abnormal position of the dislocated organs are very variable. Throughout all of these writings, however, there is a general agreement that these dislocations are- pathological. Pathogenesis of Enteroptosis. — Most of the hypotheses pre- sented in the foregoing in explanation of the etiology of enteropto- sis can not be controlled experimentally. Glenard’s hypothesis also evades critical investigation. The view of Landau that the prin- cipal and primary cause is disease of the abdominal walls is not ap- plicable to a large number of cases; for enteroptosis occurs in all ages, in men as well as in women. Personally, I have observed two cases in young girls, aged ten and twelve years respectively, and one case in a boy aged eleven. Gastroptosis, movable right kidney, and dislocation of the colon have been observed in men with strong abdominal muscles, and also in women who, although they had given birth to one child, showed no relaxation of the abdominal muscles. Therefore, the explanation of Landau is not universally applicable. Meinert’s views do not explain the exist- 7 02 ENTEROPTOSIS GASTROPTOSIS. ence of enteroptosis in men and children, and, in order to escape from this dilemma, he conceived a theory of inheritance of acquired malformations of the thorax. Langerhans (“ Archiv fiir Verdau- ungs-Krankheiten,” Bd. in, 1897) recognizes five causes, all of which are more or less familiar to us : (1) Relaxation of the abdo- minal muscles; such cases developing after childbirth he designates as Landau’s enteroptosis. (2) Hereditary enteroptotic predisposi- tion. Stiller, who adheres to this view (“Archiv fur Verdauungs- Krankheiten,” Bd. 11, p. 289), claims to have found a pathognomonic sign for enteroptosis. This is the fluctuating tenth rib , which is not firmly fixed into the cartilaginous costal arch, together with the sixth, seventh, eighth, and ninth ribs, but floats, like the eleventh and twelfth. The tip of the tenth rib, if it is floating, can be felt in the prolongation of the mammillary line. Stiller asserts that when- ever the tenth rib is mobile, there must be a movable kidney and an atonic dilated stomach. (This does not mean gastroptosis.) The reverse is not always true. Not in all cases of enteroptosis did he find a floating tenth rib. He suggests that it may be a distinguish- ing sign between congenital and acquired enteroptosis. (3) The pressure of clothing, as tight belts and corsets. (4) Chlorosis. These cases Langerhans designates as Meinert’s enteroptosis. (5) Nervous dyspepsia. The author, in accepting these five factors mentioned by Langerhans as undoubtedly active in the pathogenesis of dislo- cated kidney in its various types, would add the following : (6) Displacements of the female genito-urinary organs, produc- ing traction upon the kidney by means of the ureters. (7) Curva- tures of the spine. (8) Enlargement and increase in weight of the organ by neoplasms, cysts, etc., and, perhaps, (9) traumatism — direct violence. The most recent contribution to the pathogenesis of enteroptosis is by Joseph Rosengart (“ Zeitschr. fiir diatetische und physi- kalische Therapie,” Bd. 1, p. 220). The views of this author, which are based on sound anatomical and embryological investigations, are the following : Enteroptosis is a disposition of the abdominal viscera in such situations as are found in the fetal organism ; it is a pathological reversion to an embryonic state. This arrangement of the viscera, which is normal during fetal life, becomes still more developed during the first period of extrauterine life : i. e. } for a time after birth the abdominal organs are in a more progressed state of enteroptosis, from which the normal position of the viscera is very gradually developed. If an arrest of development at a REVERSION TO EMBRYONIC STAGE. 703 fetal stage or at a stage of very early childhood can not be accepted as an outright explanation, nevertheless the manner and order in which the organs gradually rise into the normal position in the adult point out the way and the mechanism by which enteroptosis is developed from the normal location of the viscera after this is once established. Rosengart gives a fascinating account of a study of a male fetus in the sixth month of its history. The small curva- ture of the stomach extends perpendicularly up and down, and, together with the gastrohepatic (omentum minus) and the hepato- duodenal ligaments, is directed toward the right, and anteriorly. The ascending and the transverse colons extend in a straight line from the right lower inguinal region diagonally upward through the abdomen. More than one-third of the right kidney lies upon the right iliac bone; the upper end of the right kidney does not reach so high as the left. The anterior surface of the right kidney presents a sharp edge running from the upper end to the middle of the outer margin of the kidney. Superiorly and exteriorly to this edge the kidney surface is flattened, and upon this portion rests the liver. The lower portion of the kidney, extending down- ward and inward, is pressed upon by the colon. The right kidney is separated from the spinal column by the descending portion of the duodenum. The kidney is very movable under the peritoneum, which does not cover the entire anterior surface of the organ. In the body of a child four weeks old the transverse colon was simi- larly found to extend from the lower right portion of the inguinal region in a straight line obliquely upward. The course of the transverse colon from the right inguinal region to the splenic flexure was a straight diagonal; the lesser gastric curvature was turned to the right side. The left kidney just touched the edge of the iliac bone with its inferior end ; but more than one-half of the body of the right kidney lies on the iliac bone ; its upper extremity does not touch the beginning of the diaphragm. The position of the stom- ach, colon, liver, and kidneys described by Rosengart corresponds very closely to the anatomical picture given by W. Henle of the abdominal organs in the child (“ Topograph. Anatomie des Men- schen ”), in which there is complete vertical position of the stomach, with corresponding altered position of the duodenum, the courses of the ascending and transverse colons being merged into one straight line ; the right kidney lying with its upper half on the quadratus, psoas, and transverse muscles, and with its lower half upon the concavity of the iliac bone. The under surface of the 704 ENTEROPTOSIS GASTROPTOSIS. liver, or, rather, what becomes the under surface in the adult, is turned completely posteriorly. In comparing the anatomical obser- vations on the fetus and neonatus with the autopsy reports on cases of enteroptosis, — such as are presented by Ebstein, Hayem, Aberle, Sandifort, Rayer, Schutze, Legroux, Danlos, Cuilleret, and L. Krez, — the impression will be gained that the fetal situation of the organs had continued unchanged during childhood, and throughout the entire life. As has already been stated, Kussmaul regards the vertical position of the stomach in the adult as a per- petuation of a fetal condition, and my observations on the exist- ence of gastroptosis in young children would confirm this view. The arrest of any one of the abdominal organs at a stage of fetal development is the condition necessary to create ptosis. As Rosengart points out, in order that the right kidney shall reach its correct position, and that the ascending colon shall acquire its permanent location, it is necessary for the colon to pass in front ot and over the right kidney. If this is not accomplished, and the colon remains in its fetal position, two organs are already dis- placed, and in a position characteristic of enteroptosis. The embryonic relation of the position of the ascending colon and the right kidney, and the peritoneal attachment between the two, are of great importance for the proper location of the remaining abdominal viscera. A loose attachment of the peritoneum upon the right kidney, and an imperfect transition of the peritoneum from the kidney to the colon, without completely grasping and encircling the latter, offers the condition necessaryito pathological movability for the right kidney. By means of the gastrocolic ligament the colon exerts a powerful influence on the position of the stomach. Enteroptosis is a much more frequent condition in adults than in children, which indicates that in the majority of cases the condition is acquired after the position of the viscera has approached that found normally in the adult. But even if that is the case, the primitive arrangement in the location of the abdominal organs has an important bearing on the later abnormal develop- ments. In the development of the position of the viscera to that of the normal adult the liver plays a most important role. This organ becomes relatively smaller than is found in the fetus and neonatus. In the fetus the liver extends far below the umbilicus, but in the child several weeks old it extends only to within ^ of an inch above the umbilicus. In the fetus the anterior free margin of the liver is THE ROLE OF THE LIVER IN ENTEROPTOSIS. /05 very much lower than the posterior. But in the child a few months old this posterior margin of the liver has descended still further, so that it touches the edge of the ilium, and has pushed the right kidney in front of it, on to the concavity of the ilium. With the beginning of respiration the anterior margin of the liver begins to rise, and the posterior margin descends somewhat further. The posterior and lateral sections of the diaphragm are the most mus- cular portions, which explains the fact that the pressure exerted upon the liver by the contracting diaphragm is not uniformly equal, not concentric ; for the greatest force is brought to bear upon the liver from the rear and from the sides. This effects a rotation of the liver around a horizontal axis, a line which we can imagine as extending from the right lateral to the left posterior hypochon- drium, and which runs very close to the anterior wall of the vena cava posteriorly. This rotation of the liver and the diminution of its size are accompanied by a rise of the organ ; and the remaining ab- dominal organs, which are attached to it by peritoneal folds, gradu- ally follow. When the liver has become fixed in the arching dome of the diaphragm, it is held in its position partly by the aspiration of the thorax, and partly by the hepatic veins, which attach it to the vena cava. But the most important support comes from pres- sure of the abdominal muscles. In the living being the liver is highly arched on its convex surface, and its under surface is not turned backward, but forward, and arched up also in a concave manner. This position of the liver is one of the fundamental con- ditions for the proper retention of the other viscera in normal situations. Whenever the liver is forced out of its normal position, — in which it is held by the aspiration of the thorax, by its attach- ment to the vena cava, and by abdominal pressure, — whenever this organ transiently or permanently descends, its volume increases at the same time, and it is no longer possible for the pylorus, the duodenum, and the colon to remain in normal positions. The liver is the central figure in the clinical picture of enteroptosis. Rosengart and Glenard hold this view, and Ewald reluctantly ad- mits that the liver can not be excluded from the etiology. All causes that press down the liver, — whether they act from the thoracic cavity upon the diaphragm, or externally upon the thorax, — all diseases and changes that cause relaxation of -the abdominal muscles, all diseases in the liver itself that lead to its enlargement and descent, will eventually lead to enteroptosis. The force by which the liver is retained within the arching dome yo6 ENTEROPTOSIS GASTROPTOSIS. of the diaphragm is a considerable one. Luschka compares the intimate contact of the two curved arches of the diaphragm and the liver to a great ball-and-socket joint, held together by atmos- pheric pressure, and capable of movement only in the direction of the two arched contact surfaces. The path that the liver must describe when it descends from its normal position is the same that it took when it rose to it from its fetal situation. In its descent the liver goes through the peculiar axis-rotation already described. The direction of this rotation is toward the anterior and inner portion of the abdomen. The duodenum, pylorus, and hepatic flexure of the colon will, of necessity, for anatomical reasons, have to descend with it. The posterior lower edge of the liver rises during this axial rotation and becomes superim- posed on the upper end of the kidney; and if there has been a predisposition to abnormal motility, or a loose attachment of the kidney, it will now become completely dislocated. In addition to this factor in nephroptosis another important factor is found in the new position of the ascending colon, which has to force its way over the kidney in its descent, thus separating the latter organ from the spinal column. According to this view enteroptosis may also be congenital or acquired : (i) The congenital entero- ptosis is the persistence of the fetal situation of all or of a part of the abdominal viscera; (2) acquired enteroptosis is the gradual retrograde development from the normal to the congenital or fetal position. The development of icterus in cases of right-sided nephroptosis and the frequent occurrence of gall-stones in women shortly after labor are explained by the tension of the hepatoduodenal ligament and by the altered course of the duodenum caused thereby during enteroptosis. The author has tested Rosengart’s theory by the dissection of fourteen cadavers of infants — five born before term (miscarriages) and nine born at full term. Some of the dissections were carried on by the associate professor of anatomy at the University of Maryland, Dr. J. Holmes Smith. We were enabled to confirm the positions assigned by Rosengart to the stomach, liver, and kidney of the neonatus, but all except two of the infants had a transverse colon about one inch above the umbilicus. Rosengart asserts that the ascending and transverse colons were merged into one straight line, ascending diagonally from the cecum in the right lower abdomen directly across to the splenic flexure, so that there was UPWARD DISPLACEMENTS. 707 really no transverse colon in the fetus. Of the five full-term infants we dissected, three had a distinct transverse colon and two were as Rosengart describes (/. c., p. 221). Peritonitis of the female sexual organs, and especially of their appendages, comes under consideration in connection with dis- location of the transverse colon and of the stomach. In almost all adults partial states of dislocation of the viscera, and especially of the intestines, occur so frequently that more persons have this displacement than a normal location of the intestines (Virchow, /. c). The French authors are justified in assuming the great fre- quency of these dislocations. Undoubtedly, the majority of all civilized peoples have a certain deviation in the location of their intestines, or, in other words, some slight degree of enteroptosis. While it is undoubtedly true that the majority of these dislocations are due to sinking, nevertheless the contrary is also found. There are also dislocations that move upward, in which, for instance, the splenic flexure (flexura linealis) comes to a position above the spleen immediately next to the diaphragm ; and others in which the hepatic flexure moves upward far under the liver. This upward distortion of the intestines should also receive careful consideration. It is evident, however, that every decided change in situation of this sort — especially if it is at the same time accompanied by kinking, or if considerable deviation in the direction of the intestines occurs — must bring about an interference with the passage of the con- tents of the intestines; and, therefore, nothing is more frequent than to find, at the necropsy, collections of fecal matter just at these angles and flexures, or that accumulations of gases occur, while adjacent parts of the intestines are contracted. Thus we get a picture in which spastically contracted parts of the intestines alternate with much dilated portions. The colon is the main seat of this difficulty, and the dislocation occurring most frequently is a lowering of the transverse colon, which often sinks under the navel, and sometimes even to the true pelvis, and then forms a V-shaped loop, or one with two parallel legs. The next most frequent point is the sigmoid flexure, which may show all the pos- sible varieties of descents and displacement toward the right. The two large flexures in the upper part of the abdomen — the hepatic and the splenic — are third in the order of frequency of disloca- tions. The cecum may also be drawn into similar displacements, and may sometimes move under the liver, and at other times sink down into the true pelvis. These states are relatively frequent, 708 ENTEROPTOSIS — GASTROPTOSIS. although little attention has been given to these very chronic conditions, because in life it is not known to what extent certain symptoms are connected with them, and, as a rule, no one dies from these displacements. In a treatise by Virchow (“ Virchow’s Archiv,” Bd. v) it was distinctly proved that anomalous adhesions frequently occur simul- taneously with these states ; for instance, growing together of the intestines with each other — that is, of the various curves and loops among themselves — and at other times with the adjacent organs. The hepatic flexure of the colon to a great extent be- comes connected with the gall-bladder and the whole apparatus of the evacuating gall-passages (see our illustrations of similar adhe- sions, plate XIV) ; and, on the other hand, the splenic flexure comes into close connection with the spleen and the diaphragm, and the iliac flexure with the sexual organs, especially in women. These reciprocal relations undoubtedly produce pulling of the various parts among one another. The relation of partial peritonitis to visceral dislocations is more difficult to understand, and in this respect two conditions are to be distinguished — namely, a primary one, in which peritonitis occurs earlier, and a secondary one, in which, conversely, the peritonitis is caused by the dislocation and by the other processes going on within the adherent part of the intestines. Concerning the first, we have a clear example in the recognized cases of circumscribed peritonitis, which are caused by processes starting from the gall-bladder (perihepatitis, peritonitis cystica), when adhesions are formed within the environment of the gall- passages ; this is followed by a shifting of the parts among one another, since the adhesive masses gradually contract and the retraction proceeds further and further. On the other hand, secondary peritonitis is much more difficult to prove in cases in which one is confronted with the completed process ; one can only recognize it when fresh processes still exist. These are found chiefly in those cases when inflammation of the mucous mem- branes, extending to the peritoneum, causes a bending or kinking of the intestine. Virchow was the first to draw attention to the facts in studies on dislocations with so-called diphtheric dysentery, which may appear distributed in a variable manner, so that the foci of inflammation are separated by long stretches of normal mucous membrane. Apparently normal sections are succeeded by new areas of very PERITONITIS AND COLITIS AS CAUSES. 7O9 severe disease, so that one may distinguish a sort of interrupted localization. He suggested that the anomalous flexure, just as the normal, is in itself a motive for localization, in that it brings with it a retardation in the passage of the contents of the intestines, which contain injurious substances that react upon the mucous membrane, and from which the irritative process is developed. It is exactly the same thing that we see in stenoses, where further disturbances arise above the obstruction, or with incarcerated herniae, where the inflammation develops in the part of the intestine above the incarceration, and sooner or later extends to the peritoneum. These consequences (secondary peritonitis) of partial enteropto- ses due to acute inflammations are easily recognized (“Arch. f. pathol. Anat. u. Physiol.,” 1871, lii, 34). Enteroptosis is not an anatomical process connected with con- stant clinical symptoms. On the contrary, the symptoms will probably be manifold, according to the special pathological circum- stances occurring in various cases. Accordingly, the disease in each case will, to some degree, come under different categories, and one may not bring diphtheric or simple colitis, developed in anomalous flexures, into the same category as dislocation pure and simple ; these are two very different things (Virchow). I, therefore, do not consider enteroptosis an entity, but prefer to divide it into several groups of diseases when it is regarded symptomatologically and therapeutically. We are dealing here with very common deviations, and, if we could count the cases, they would be found to be more frequent than the normal state ; the less complicated dislocations only from time to time become the origin of severer symptoms. Leshaft has shown that the size and fullness of the abdominal organs, as well as the condition of the abdominal integument, are important for the reciprocal conduct and relation of the intra- abdominal organs. Every abnormal fullness or increase in size of one of these organs, as well as a decrease in the power of resistance within the compass of the abdominal integuments, will produce a change in location — a sort of ptosis, in the sense of Glenard. It has been proved that a descent of the transverse colon, especially the right flexure, carries with it a lowering of the stomach and a descent of the right kidney. It is evident that the transverse colon does not descend spontaneously without pathological causes, so that 7io ENTER0PT0SIS GASTROPTOSIS. there can not well be a primary enteroptosis. It is caused by etiological factors, such as abnormal adhesions, change of con- tents (coprostasis), anomalous flexures (Virchow), tumors, perpetua- tion of, or reversion to, a fetal condition, etc., by which the trans- verse colon is pulled down, and with it, secondarily, the stomach and small intestine, and eventually the kidney, especially on the right side. Therefore most enteroptoses are of secondary nature. Dislocation of the Kidneys. — In 1887 Litten first emphasized that “ in the anomalies of location of the kidney one must sharply distinguish dislocation and movability.” Although both irregu- larities often occur together and simultaneously, there is no organic necessity for the same ; rather, both processes may ap- pear entirely independent of each other, although in many cases one finds a dislocated and a movable kidney in the same individual. Renal displacements may be (1) congenital or (2) acquired. Con- genital displacement occurs more frequently with the left kidney, and oftener in males than in females. (The ratio of Stern is 20 : 9.) It rarely occurs in both kidneys, except in those cases in which they have grown together. These kidneys are found in the pelvis or above the promontory of the sacrum, and are often associated with intestinal and genito-urinary abnormalities ; but as the con- dition gives rise to few symptoms, it has more of a pathological than a clinical interest. The diagnosis is difficult unless the mass can be palpated from the rectum or vagina, or unless fluid can be aspirated from it, giving the reactions of urine. The acquired renal displacement is (1) due to tumors in the neighborhood of the organ, or (2) due to abnormal movability, assigned to various causes already mentioned. In both congenital and acquired dis- placements the abnormally situated kidney may be fixed or mova- ble. Congenital displacements are, as a rule, fixed ; the acquired show a variable movability. A movable kidney may be ( a ) in a normal position or ( b ) dislocated ; a dislocated kidney may be ( a ) movable or ( b ) fixed. The so-called floating kidney (Wander- niere) belongs to the second type, variety a; it is a dislocated, movable kidney. According to Kuttner, Litten, and Ewald, four distinct phases or degrees of nephroptosis may be differentiated by palpation : (1) A respiratory movability without dislocation. (2) Respiratory mov- ability with slight anterior dislocation — one-third to two-thirds of the kidney can be palpated ; this is termed a “ dislocation of the first degree.” (3) Respiratory movability with close approximation MOVABI LITY AND DISLOCATION. 7 ii to the anterior abdominal wall. The kidney is palpable in its entirety, and can be easily moved about; this is termed a “ disloca- tion of the second degree.” (4) The dislocated kidney is firmly adherent in its abnormal position. Litten distinguishes the following relations concerning the loca- tion and movability of the kidney : First, a simple dislocation of the same; this is more frequently congenital than acquired. The con- genitally dislocated kidney is found more frequently on the left than on the right, and with approximately equal frequency in men and women. Often both organs are dislocated. Not taking into account the most frequent form of dislocation, — the so-called horseshoe kidney, in which both organs are united into one, — the dislocated kidney is found either close under the bifurcation of the aorta, or above the promontory of the sacrum, or, finally, above the sacro-iliac synchondrosis. With the change in location there is almost always connected an anomaly of the origin or course of the renal artery, while the suprarenal capsule more frequently remains in its place and does not follow the kidney to which it belongs. Congenitally dislocated kidneys are almost always fixed in the place of their dislocation. An exception to this is the movable horseshoe kidney. Acquired dislocations of the kidneys are chiefly due to patho- logical enlargements of neighboring organs (spleen, liver, pan- creas, suprarenal capsule), and are found higher or lower than the normal and nearer to or further from the vertebral column. The pressure of articles of clothing (such as corsets, belts, girdles, etc.) seems to have considerable influence, by which the liver, and with it the kidney, is pushed down. Consequently, this anomaly of location is found less frequently left than right — more frequently in women than in men. By the sinking of the liver — e. g ., in con- sequence of hydatid cysts — the kidneys may be completely turned around, as a result of which one may feel the inner edge with the hilus upward, the convex edge downward, or pointing in some other abnormal direction. Most frequently in this form of disloca- tion one finds the kidney pushed downward and inward : i. e., toward the median line. This form of dislocation of the kidney, acquired late in life, may become movable; it is almost always replaceable if it has not become fixed in its new location by secondary inflammation. While one might describe the above-mentioned forms as dis- location of the kidney with and without movability, we now 712 ENTEROPTOSIS GASTROPTOSIS. come to the forms in which the movability plays the main role, — dislocation of the secondary kind, — movable kidneys with and without dislocation. Here we have to distinguish two main classes: (i) the wandering or floating kidney; ( 2 ) the movable kidney. The floating kidney is distinguished by the mesonephron, — a mesenteric fold fastened to the kidney, — which generally consists of two plates, between which the organ is held and with which it is surrounded. The characteristic of this form is not the abnormal position, but the ability to change one abnormal position with others, to reach extreme positions, and even to reach the normal position again, of itself. The presence of this anomaly is always to be traced back to a congenital disposition of the peritoneum, with consequent stretching of the renal vessels. Generally, one finds at the autopsy in these cases that all the folds, protrusions of the peritoneum and mesenteries, are abnormally long and lax, and the- foramen of Winslow is very wide, corresponding to the laxity of the lesser omentum and the duodenal-hepatic ligament. If one uses this anatomical arrangement for the classification, and does not designate at will every unusually mobile kidney as a “ floating ” or “ wandering kidney,” as is frequently done from a clinical point of view, it is evident that every floating kidney, in the sense adopted by Litten, must be congenital. It will hardly be possible, therefore, during life to distinguish these two processes from each other ; on the other hand, there will also be cases in which a very short and tight mesonephron will restrict the extent of wandering of the floating kidney. A simultaneous permanent dislocation of the kidney may be present, but not necessarily; it happens, occasionally, that a floating kidney in the course of time becomes fixed and permanent in any abnormal location by means of perinephritic processes, so that in spite of its mesentery it is no longer movable. Litten has reported a considerable dislocation in a wandering horseshoe kidney, where one portion of the organ lay in the right inguinal region, while the opposite part lay upon the horizontal ramus of the right os pubis. The organ could be pushed about within the widest limits, and it also moved spon- taneously, causing unpleasant sensations to the patient. In this intraperitoneal position of the kidney the organ seems to lie imme- diately under the abdominal integuments, where one can not only palpate it, but can sometimes also recognize its contour distinctly through the abdominal integuments. Percussion over the organ ETIOLOGICAL FACTORS. 713 produces in these cases a distinct dullness, not a tympanitic sound, as in the case with the kidney situated extraperitoneally. The movable kidney is distinguished from the normal solely by an excessive movability, which is revealed to a greater or less de- gree (not taking into account the normal respiratory movability) in changes in the position of the body. Often this anomaly is acci- dentally recognized in manipulations instituted for the examina- tion of the abdomen. A dislocation of the kidney can and often does exist simultaneously with the above-mentioned condition, but it does not necessarily have to exist. We find the right kidney more frequently movable than the left (the proportion being 15 to 1), and the anomaly is more frequent in women than in men (the proportion being 84 to 16). The degree of movability seems to be chiefly dependent upon the varying laxity of the part of the peri- toneum descending in front of the kidney, as well as upon the abundance or absence of the perinephritic or subperitoneal adipose tissue in the region of the loins, and the greater or lesser power of resistance of the intra-abdominal organs, including the abdominal integuments. One can often feel the kidney so distinctly that it may be palpated with anatomical exactness, although it lies extra-peri- toneally, separated from the anterior abdominal wall by intestinal loops; consequently it gives forth a decided tympanitic sound, although one can press it very close to the abdominal wall. The degree of movability is just as variable as the degree of dislocation ; in most cases we find only slight dislocations from the normal posi- tion, downward and inward. In by far the greater number of cases this condition is acquired, especially in the years between twenty and forty. Etiologically , the following factors seem to have the greatest influence: The disappearance of the fat in the adipose capsule in which the kidney is held — through this the kidney becomes mov- able in this capsule; the disappearance of the perinephritic adipose tissue, through which the kidney, and also its fat capsule, are moved out of place; further, the laxity of the peritoneum, the increase in the weight of the liver, together with the respiratory displacement of the same, prolapse of the uterus and of the vagina, neoplasms and retroflexions of the uterus, herniae, weakness and laxity of the abdominal walls, and, above all, the much-discussed enteroptosis. Also heavy lifting, coughing, pressing, repeated pregnancies, vom- iting, as well as traumatism and violent agitation, are given as ENTEROPTOSIS — GASTROPTOSIS. 7H causes. One of the most frequent causes for the movability of the right kidney seems to be lacing with corsets, belts, and girdles. Thus, von Fischer-Benzon, in his dissertation from the pathological institute at Kiel, states that in twenty-one cases of movable kidney there was found in eleven cases a furrow in the liver due to lacing. By lacing a decided pressure is exerted upon the lower part of the thorax, by which this is greatly narrowed and the organs lying within it compressed. The liver, being the largest and least com- pressible of these organs, will suffer especially. The liver, and the kidney closely connected with it, are pushed down, and the latter must participate in the respiratory excursions of the liver. The more frequent displacement of the right kidney is partly explained by the anatomic arrangement of its blood supply. The left kidney has a shorter renal artery and a tighter attachment to the suprarenal body, by means of the suprarenal vein, which on the left side opens into the renal vein. H. Schmid (Penzoldt and Stintzing’s “ Handbuch d. Therapie,” Bd. vi, S. 345) regards the renal vessels as the most important attachments of the kidney ; if the vessels are abnormally long, an essential support is lost. L. Knapp (/. cl) looks upon uterine displacements and consequent dragging upon the ureters as a frequent cause. Since the respiratory movements of the diaphragm are com- municated to the kidney, the respiratory movability of the kidney may be regarded as physiological. The author, following the observation of James Israel, has convinced himself of this normal movability at operations. Method of Palpating the Kidneys . — The chances of feeling the respiratory movability of the right kidney will vary according to the relaxation and the degree of resistance of the abdominal integuments, the control and experience of the patient in breath- ing, and according to the manual dexterity of the examiner. It is especially important that the patient inspire deeply ; this can be learned easily enough by practice. The knees and thighs of the patient must be flexed. The examiner himself must not cause any pain or tension of the abdominal integuments by his manipulations. It will then be possible in many cases, by means of the bimanual method of examination, to feel the kidneys, espe- cially the right one, as it is more easily palpable. It would, how- ever, be entirely false to believe that one could prove the respira- tory movability of the kidneys in females only, and especially in PALPATION OF KIDNEYS. 715 multipart. On the contrary, it may be shown with the greatest distinctness in men and girls, and even in small children. In bimanual examination, in order to feel the right kidney the left hand is placed immediately in the rear, under the edge of the ribs on the right side, while the tips of the fingers of the right hand, similarly placed together, take the corresponding position at the lower arch of the ribs on the same side ; on gradual downward pressure one feels a larger or smaller part of the organ between the fingers during deep inspiration. The deeper the inspiration, the greater the portion of the kidney that becomes palpable, until with forced inhalation one may sometimes feel the whole organ pressed out under the arch of the ribs, and can, with the greatest distinct- ness, examine it by palpation between both hands. If the fingers of both hands are pressed together, the kidney escapes from the hands (this is a characteristic sign), and the person examined feels a slightly unpleasant sensation, and sometimes a decided sensation of pressure or pain, or a distinct jerk. The difficulties in the way of kidney palpation have, in the author’s experience, been very adipose abdominal walls, tightly contracted recti muscles, fecal accumulations in the colon, and, rarely, neoplasms of the gall- bladder and colon, hydatids of the liver, and causes enlarging or lowering the liver, or separating a portion of the lower edge by a furrow due to compression. With this method of examination one may get a precise conception of the size, consistency, and thickness of the organ ; possibly of neoplastic formations, lobulations, irregularities, even granulations and processes of shriveling, and especially of increase in consistency, size, and diameter. The looser the abdominal in- teguments, and the more completely the condition of enteroptosis is developed, the more favorable are the conditions for palpation. If the kidney can not be palpated when the patient is in the dorsal position, I have frequently succeeded in palpating it by placing the patient on her hands and knees in bed. The examiner stands on the left side of the bed and patient, facing the head. Both arms are passed around the patient’s body ; the right hand is in- serted beneath the lower edge of the liver while the left seeks to meet it by pressure from a point about two inches above the umbilicus. Gastroptosis. — Diseases of the stomach are frequently con- nected with dislocation and movability of the kidney. Ewald and others are of the opinion, supported by observation of numerous ENTEROPTOSIS GASTROPTOSIS. 7l6 successive cases, that the frequency of gastrectasia with dislocation of the right kidney is due to an etiological connection. The view taken by Quincke, Nothnagel, and Leube is that both patho- logical processes occur, indeed, very often side by side, without any causal connection necessarily existing between them. I have not seen an undoubted case of dilation of the stomach due to obstruction of the pylorus or duodenum by floating kidney. I have observed gastroptosis and nephroptosis occurring together in numerous cases — the combination being due to the same cause. The changes of position (after descent) of the stomach in consequence of so- called enteroptosis and dislocation of the right kidney are not the classic gastrectasias that develop in consequence of mechanical obstructions at the pylorus (new formations, cicatrices of ulcers, distortions in consequence of adhesions, compression, obliteration, kinking, etc., page 231 of the “Proceedings of the German Con- gress for Internal Medicine,” 1887), but consist in the insufficiency of the pylorus, with deep location and dilation of the stomach, because the pylorus and the duodenum frequently retain a normal position. If one does not take into account the gastrectasias resulting from mechanical causes, there still remains a very large number of functional disturbances of the stomach, which lead, further, to insufficiency of the musculature and to dilation and low position of the organ. To this class are assigned : 1. Disease of the musculature of the stomach in consequence of protracted chronic gastritis. 2. Excessive exertion of the stomach in consequence of exces- sive amounts of healthy food or unsuitable indigestible food. 3. Abnormally slow peristalsis with retention of food, as well as the abnormal decomposition of the retained ingesta, with exces- sive formation of gases. As a result of these various chronic pathological conditions of the stomach, each of which singly forms only a link in the whole chain, a dilation of the stomach, with attenuation of the walls, finally develops, and later a sinking down of the organ and descent of the right kidney, with abnormal movability. The function of the stomach is seriously injured in many directions, especially the motor power, which under some circumstances ceases entirely. In such individuals 200 c.c. of liquid food are often found in the stomach from seven to eight hours after ingestion. Such con- ditions (called by the French “ dyspepsie des liquids ”) concern only liquid food, while solid foods are digested, though much CAUSES OF ENTEKOPTOSIS. 717 more slowly than normally. It was thus possible to effect a nearly normal digestion of discs of albumin placed in the gastric juice pumped out of the stomach. These observations are more intelligible in the light of von Mering’s experiments (see part first), according to which it is certain that no ab- sorption of water takes place from the stomach, even normally; and for the resorption of substances that can be taken up by the mucosa, a return secretion of liquid takes place from the mucosa into the stomach. So that it sometimes happens that after six or eight hours more liquid is drawn out of the stomach than was in- gested. The digestive power varies in these cases with the state of HC 1 ; it may be fairly good, but it may be entirely absent. There are undoubtedly cases of gastroptosis in which the dislocated stomach functions normally. The displacements of the intestines, which arise through circum- scribed peritonitis, through obstruction of the feces, etc., were de- scribed by Virchow as early as 1853. Glenard and Ewald have made reference to the entirely uncomplicated, one might say the purely gastric and intestinal, cases. The suggestion of Landau, not to be content with the diagnosis of the movable kidney, floating liver, and kinking of the transverse colon, but to seek the etiological diagnosis, in order not to come to the incorrect conclusion that we have to do with independent diseases, would be valuable if it were easy of execution. In the author’s opinion, the etiological diagnosis is difficult, sometimes impossible. Enteroptoses, etc., are secondary states, and should, for diagnosis and treatment, be considered in the same light as roseola occurring with typhus or syphilis, in which one is cer- tainly not content to diagnose roseola simply, but adds typhus or syphilis with roseola. Causes. — The diseases that cause a sinking of one or more of the abdominal organs are all those which absolutely or relatively increase the capacity of the abdomen, and thus allow the large in- testine, fastened by the relatively long mesocolon, to sink, accord- ing to its weight. The simplest or first degree, for instance, may be said to exist when we meet with a light inguinal, femoral, or umbilical hernia. In this case all the intestines not in the hernial sac may sink, through pulling and dragging. Since the portions of the intestines which were formerly in the peritoneal cavity have come out, the capacity of the abdomen has been relatively in- creased. 7 i8 ENTEROPTOSIS — GASTROPTOSIS. It is true, splanchnoptosis is not a necessary consequence of large ruptures. When the elasticity and contracting power of the abdominal integuments are very great, they may counteract the increase in volume by tonic contractions. A number of cases are reported in which almost all the intestines lay in ruptures; and in spite of this, the kidney, liver, and uterus were approximately in normal positions. The abdominal integuments were contracted tightly inward and were concave. Of far greater importance for the origin of all kinds of entero- ptoses is a second great category of diseases — namely, all wasting diseases , which produce a quick consumption of the fat of the body, and also disturbances in the nutrition of the abdominal integu- ments. Thus, after typhoid fever, scarlet fever, and other infectious diseases, splanchnoptoses of all kinds, such as dislocation of the kidneys and of the liver, etc., have been recognized. It is evident that the transverse colon must be lowered also when the liver and kidney can be felt to have descended, for the transverse colon, lying under these organs, and connected with them directly and indi- rectly, can not retain its position under these conditions. To prove the descent of the transverse colon in such cases, the method of the injection of air into the stomach and into the colon alternately (Ewald) is not always necessary, nor the very doubtful direct palpation of the transverse colon, as given by Glenard. Chronic diseases, such as phthisis, produce exactly the same effect as acute diseases ; and Landau holds that primary nervous dyspepsia, primary chronic gastritis, duodenitis, etc., are fre- quently not the result of enteroptosis, but, by means of the disappearance of fat and weakening of the abdominal integuments, causes of it. Individuals may be examined at one period of indis- position and no sinking of the liver and kidney can be demon- strated, but if they should acquire an ulcer of the stomach or nervous dyspepsia, with disturbances of nutrition, we may be able to show prolapse of the liver or kidney in the later course of the disease. Among the patients observed by us — sufferers from disturbances of nutrition, nervous dyspepsia, emaciation, etc. — in which the splanchnoptoses were demonstrated, there were a number of cases in which the disturbances of nutrition caused the ptoses, and not the reverse. In five cases the patients had been closely examined repeatedly before, and signs of enteroptosis were discoverable ; in later years these had become very evident. STENOSING OF INTESTINES. 7 1 9 Relaxation of the abdominal muscles , with or without pendulous abdomen, is a frequent cause of splanchnoptosis. Sinking of the kidneys and liver develops in women from whom large ovarian tumors or myomata^ have been removed by laparotomy. Other cases of pendulous abdomen are acquired by repeated and rapidly consecutive births , and by unsuitable treatment during and after confinement. Similarly, splanchnoptoses will appear in individuals who suffer from ascites , and who have been punctured repeatedly, and in whom the abdominal muscles have finally become paretic on account of abnormal fullness and distention. The typical form of pendu- lous abdomen does not always arise in these cases. If the support of the abdominal viscera, formed by the abdominal integuments, becomes insufficient, the intestines follow the law of gravitation and descend the length of their mesenteries, the peritoneal folds of the liver and kidney relax also, and these viscera descend, because one of their main supports — namely, the intestinal mass — has been withdrawn. That which is principally and etiologically of prime importance in these particular cases, therefore, is not the sinking of the transverse colon, but disease of the abdominal integuments. There are five places especially at which stenosing phenomena may appear through temporary kinking : 1. At the pyloric part of the stomach, or where the duodenum passes over from the superior horizontal part into the vertical portion, which is tightly joined to the spinal column. 2. At the entrance of the jejunum into the duodenum, at the duodenojejunal flexure (E. C. Perry and L. E. Shaw, “ Diseases of the Duodenum,” “ Guy’s Hospital Reports,” 1893, p. 171). 3. At the transition of the small intestine into the fixed portion of the cecum. 4. At the transition of the transverse colon into the descending colon, which is comparatively tightly fixed at the posterior lateral abdominal wall, and is further attached high up into the left hypochondrium by the phrenocolic ligament (Phoebus). The left flexure of the colon normally forms a right angle, which, however, becomes an acute angle in patients with pendulous abdomen. 5. In some cases, when the hepatic flexure of the colon has not sunk, stenoses may develop in it at a corresponding place, as de- scribed in No. 4 (Landau, on “ Pendulous Abdomen,” p. 82, et seq.). The floating kidney is to be put semiotically on a level with enteroptosis ; it is not a disease sui generis. 720 ENTEROPTOSIS GASTROPTOSIS. The dangerous sequences of floating kidney are hydronephrosis, intermittent hydronephrosis, and incarceration of the kidney (first described by Dittl). This dangerous condition is largely ascrib- able to compression of the renal veins. Diagnosis. — Movable kidney may be undoubtedly recognized in all cases where we can firmly grasp it between the fingers, and can thus determine exactly its entire configuration. Secondly, the diagnosis is comparatively simple in those cases when we may not determine the configuration, it is true, but when we discern only a smooth, movable body, often movable only within narrow limits, if we are aided by the instructions of the patient, that after bodily exertion, this body was suddenly felt. But there are cases where this information of the patient is lacking, where we can not make the diagnosis by palpation with certainty, and here mistakes are possible. An error which has occurred repeatedly, according to our experience, is to mistake a small lower part of the liver, sepa- rated from it by a strong furrow due to compression, which part, on account of the depth of the furrow, seems to be movable, for a floating kidney. Guttmann has seen such cases repeatedly in autopsies, which during life were regarded as movable livers. Osier (“ Lectures on the Diagnosis of Abdominal Tumors,” p. 97) gives an illustration of a tongue-shaped prolongation of the anterior mar- gin of the right lobe, with the gall-bladder projecting below it. By means of the bimanual examination, which has been described in detail, we are, at least in a large number of cases, able to feel the lower end of the right kidney during inspiration. And since abnor- mal (extreme) movability occurs most frequently with the right kid- ney (in more than eighty per cent, of the cases), therefore, by finding the right lower edge of the kidney in bimanual palpation, the error of mistaking a portion of the liver (separated from it by a furrow) for the kidney should be avoidable. Proving by means of percussion that the kidney is not in the proper place is very unsatisfactory. It seems, indeed, in some cases, that the dullness is less on that side where the kidney is wanting, than on the opposite side, where the kidney is present. But in most cases of movable kidney there was no difference in the reso- nance in the region of the loins on either side. We therefore attach no value to the results of percussion in the diagnosis of dislocated kidney, and the same opinion of the use of percussion holds good in diseases of the kidney in general. Only in isolated circumstances it may aid the other methods of examination, — e.g., FREQUENCY OF NEPHROPTOSIS. 72 I in cases of great swelling of the kidneys, — but in most cases per- cussion of the kidneys is entirely worthless, and hence I do not consider it a diagnostic method. Frequency of Dislocated Kidney . — The statements of various clin- icians concerning the frequency of floating kidney vary consider- ably. Lindner stated that it was the most frequent abnormality of the female body, and that one woman in five to seven was afflicted with the trouble. Edebohls gives 18 per cent., Mathieu 27.1 per cent., Fischer-Benzon 17 to 22 per cent., John Schmitt 10 per cent. (New York, “ Medic. Monatsschrift,” March, 1891). Ludwig Knapp (“ Wanderniere bei Frauen,” Berlin, 1896) gives 5 per cent. Einhorn gives 1.8 1 per cent, for men and 20 per cent, for women (“ New York Med. Record,” Aug., 1898). As far as our clinical material permits us to judge (260 examina- tions of females from hospital and private practice), the rate for our Baltimore cases is six per cent. The right kidney is dislocated more frequently than the left, the proportion being 15 to I, and bilateral dislocation was found only once. This rate includes only strictly dislocated kidneys, not palpable, nor even movable, kid- neys. Twelve cases in which the organ could be moved up and down within a space of from 1 to 1 y 2 inches approximately were not included ; they were found in females giving no signs or symp- toms of abdominal disease, being in the hospital for acute pul- monary diseases, injuries, and throat inflammations. A fundamental requisite in describing these conditions is to distinguish precisely between (1) palpable, (2) movable, and (3) dislocated kidneys. The last may be ( a ) movable — i. e., the so- called floating kidney — or ( b ) immovable : i. e. y anchored down in its abnormal position. (See classification on p. 710.) Unless unusually adipose abdominal walls or firmly contracted recti muscles interpose between the palpating fingers and the kidney, the latter should always be palpable : i. e. } one should be able to feel the kidney in about fifty per cent, of all cases. Fur- thermore, these palpable kidneys should, even in the majority of cases, be made out as mobile, for these organs, especially the. right one, are normally mobile to a slight degree. James Israel has observed the respiratory movements of the kidney in a case in which the lumbar regions had been opened. In animals (dogs) the author has never observed a movable kidney under normal conditions; this is accounted for by the horizontal position of the body. But in human beings the right kidney was slightly 722 ENTEROPTOSIS GASTROPTOSIS. movable in fifty per cent, of our cases. Palpable and movable kid- neys, as a rule, give no symptoms — only the various types of dis- located kidneys are clinically important. Occasionally, the kidneys can not be palpated in highly nervous individuals, because of con- traction of the recti ; if it is absolutely necessary to locate the kidneys in these cases, they should be examined in a warm bath or under narcosis. Dislocated kidneys are such as can be moved out of their nor- mal position more — i. e ., further — than any distance ascribable to the normal respiratory movability, and that can exchange one abnormal position with another or with the normal, and that give rise to abnormal symptoms, as a rule. A kidney that is movable in its adipose imbedding from one to two inches is not yet dislo- cated, and symptoms due to torsion of the ureters and vessels do not arise until the mobility exceeds that limit. Great accuracy and precision are needed in the use of the terms palpable, movable, dis- located, and floating kidney, and there must be some consensus or agreement concerning the clinical meaning of these words, and some limit to their significance, before statistics can have any value. Up to the present, this matter is in a state of confusion. The degrees of dislocation schematically given on page 710 may aid us in reaching an understanding. Ewald’s assertion of the extraordinary frequency of movable kidney is the more astonishing because in autopsies one does not often find movable kidneys. Guttmann, in reporting his experience, resting upon about 8000 autopsies at Berlin, which for the most part he himself noted down, stated that in these autopsies the float- ing kidney was not frequent. His experience agrees with that of the pathological institute of the Charite, Berlin. Landau, in his monograph on the floating kidney, states that in the Charite float- ing kidneys were found very rarely at autopsies. It may be added, however, that in a horizontal position the movable kidney sinks back to its normal position, and is, therefore, liable to be overlooked in the necropsy ; but the movability must persist, and this must attract attention when the kidney is taken out. In taking out the kidney an experienced dissector will notice at once whether it is normally fixed or movable, dislocated, or fixed in an abnormal position. The explanation given by Neumann of the scarcity of floating kidneys at autopsies, that the fatty envelop, becoming solidified after death, tends to fix the kidney, is unsatisfactory. In the first place, the fatty envelop, if there is any left, is not any more SYMPTOMS OF GASTROPTOSIS. 723 solid after death, necessarily, than before, because rigor mortis does not affect the solidity of fat; this is influenced only by the tempera- ture of the cadaver. But Oppolzer, Ebstein, and others assign loss of the fatty imbedding as a cause of floating kidney, and any one who has observed a nephrorrhaphy can assure himself of the scarcity of fat about such dislocated organs. Besides, it requires a power- ful effort of the imagination to conceive of replacement of a kidney (dislocation of the second degree) that may be as far as ten inches away from its normal position by solidification of a supposed fatty envelop. Reversal of the Location of the Viscera {Situs viscerum inversus ). — In this state the stomach lies normally on the right side, the heart on the right side, the liver on the left. The site of all the viscera is exactly reversed ; there is a situs inversus , however, in which the heart is found in the normal position at the same time; the location of all other organs is reversed. Vertical position of the stomach is an anomaly frequently associated with atony, and is attributed to tight lacing. It becomes important clinically only when the motor function is interfered with, in which case the treatment is the same as that for motor insufficiency. The diagnosis of vertical stomach should present no difficulties when the methods stated on pages 98 to 112 are employed. Symptoms of Gastroptosis. — The symptoms are brought on by the gastric and intestinal atony, by the mechanical disturbances caused by the descent of the organ, and neurasthenia. We have observed a number of cases of gastroptosis that presented no diges- tive symptoms whatever. The dyspeptic symptoms that are most common are : pressure, fullness, distention, and pain (gastralgia), coming on at irregular intervals, and independently of the digestive act or of the quality and quantity of the food. A sensation of heat or burning at or below the umbilicus is at times described. Eruc- tations, nausea, vomiting, and pyrosis may be complained of. Chronic constipation is a typical accompaniment ; flatulence and occasional attacks of diarrhea alternate with constipation. When there is an evident coloptosis, a very stubborn membran- ous dysentery is, as a rule, present ; being, no doubt, caused by abnormal kinking and stenosing flexures in the course of the large intestine. The quantity of the urine may be very variable, and depends upon the permeability of the ureters. Absolute obliteration of the ureter by kinking may produce oliguria or anuria, which may be 724 ENTEROPTOSIS GASTROPTOSIS. followed by profuse urination when the ureter becomes straight- ened. Cirailatory Symptoms . — A low blood pressure in the systemic vessels is characteristic of this disease. Disturbances in the rhythm and rate of the heart-beat are common. Tachycardia after evacuation of the bowels I have also observed frequently. Nervous Symptoms . — The typical clinical picture of aggravated neurasthenia is frequently associated with these cases. The mani- fold pains complained of during bodily exertion are referable to drawing and tugging upon the nervous apparatus supplying the dislocated organs. Intense lumbago is a most frequent sign. The spleen has been very rarely found dislocated in splanchno- ptosis, Glenard having observed splenoptosis only twice in 148 cases. Hepatoptosis can be recognized by a lowering of the area of hepatic dullness. There are several degrees of liver displace- ment : (1) A portion of the liver projects beyond the arch of the ribs into the abdomen, and the upper border is correspondingly lower. (2) The lower portion, from y 2 to of the liver projects into the abdomen ; the liver dullness above the edge of the ribs is reduced to a narrow zone or is entirely absent. (3) The entire liver is located within the lower abdomen. Coloptosis. — Descent, displacement, with consequent local sten- osis, and dilation of portions of the colon can be recognized by distending the colon with air or water. The air is usually forced in through a long colon tube (Langdon) by means of a double-bulb pump, or from 600 c.c. to one liter of warm water are gradually allowed to run in under gentle pressure. Normally, a distended area is palpable, and even visible, two or three inches above the umbilicus; the ascending and descending colon can be recognized as two arching elongated prominences about three inches to each side of the umbilicus. When the colon is prolapsed, the transverse portion is found touching at the symphysis pubis, or even within the pelvis. I have occasionally observed that a prolapse of the colon was recognizable by the distention that had occurred through gaseous fermentation, and that artificial distention was unneces- sary. When a prolapsed colon is distended with warm water, it changes its position with the attitude of the patient. Thus, a colon that rests on the symphysis will rise to its normal location when the pelvis is elevated and the thorax depressed. If this does not occur, the colon is adherent in its normal location. Idiopathic dilation of the colon may give rise to symptoms that COURSE OF GASTROPTOSIS. 725 may cause confusion in differentiating the location of stomach and colon. Reginald H. Fitz called attention to the similarity in the clinical histories of chronic phantom tumor and that of idiopathic dilation of the colon (“Am. Jour. Med. Sciences,” Aug., 1899, p. 134). The methods given will suffice to determine the location and capacity of the colon as well as that of the stomach. Electrodiaphany is an available method of diagnosing the course and location of the colon. The author has frequently used it for that purpose (see pp. 104 to 112). The results and conclusions derived therefrom are subject to the same limitations as when the electrodiaphane is used within the stomach. Gastroptosis can occasionally be recognized by inspection ; the methods described in chapter xi, pages 98-104, if systematically carried out, can leave no possible doubt regarding the existence of this dislocation. The differentiation between prolapse and dila- tion is facilitated by electrodiaphany. If the stomach is dilated, not prolapsed, the transillumination area will exhibit respiratory mov- ability. Ewald, Litten, and Bartels assert that dilation of the stomach frequently occurs, with nephroptosis or hepatoptosis ; this is not confirmed by Boas. Myasthenia, with overretention and stasis of ingesta, is frequently observed, though not in all cases of prolapse of the stomach. The typical clinical picture of classical dilation may occur in connection with gastroptosis. By insuffla- tion and coating of the stomach with subnitrate of bismuth by means of the intragastric powder-blower the size and location of the organ can be demonstrated by means of the Rontgen rays. Analysis of the gastric contents in gastroptosis, though yielding few practical aids to diagnosis, is useful in selecting a proper diet. The results of such chemical analyses are variable. The course of gastroptosis is protracted and generally chronic. Great feebleness, abnormal sensations of pain and compression, or of cold and hot aurae, indisposition to exertion, and faintness are among the most common symptoms in this most variable clinical picture. Severe disturbances of nutrition and anemia unfailingly appear as the digestive distress continues. The points of differentiation between falling of the stomach and dilation and atony have been considered in the chapters on these diseases. The differential diagnosis between the symptoms of gastroptosis and nervous dyspepsia is difficult, sometimes requiring all the ingenuity of an experienced diagnostician. This is prin- cipally because the symptoms of both states are occasionally 48 726 ENTEROPTOSIS GASTROPTOSIS. identical, and because gastroptosis is often associated with nervous dyspepsia. The state of the peristalsis is normal in nervous dys- pepsia, but in gastroptosis there is, as a rule, a myasthenia, with overretention of ingesta. Treatment of Gastroptosis. — Prophylaxis . — The frequency of gastroptosis and enteroptosis in women demands that the physician should emphatically oppose tight lacing, or any garment that con- stricts the waist. The dresses should be so constructed as to be supported from the shoulders. We have already spoken of this under the heading of acute gastritis. If possible, the modifications in dress should be made in accordance with the rules of fashion. It will do no good to oppose the unrestricted domination of this tyrant of the female sex, without clear indications of the benefit to be derived. We have already emphasized the fact that a properly con- structed corset does not necessarily work harm, but may eventually be useful, by the support it gives to the back and breasts. The dresses should, however, be supported from the shoulders. It is necessary to do this before the enteroptosis is developed. The relaxation of the abdominal muscles must be prevented by using well-applied bandages after confinements, worn for several months. The bowels must be kept regular. Massage, electricity, and cold-water applications may contribute to a vigorous abdom- inal musculature, but the most effective method of strengthening the abdominal muscles is by abdominal gymnastic exercise. (See Illoway, “ Constipation.”) We will briefly describe two of the most practical methods of training the abdominal muscles : No. i . — The patient places himself on a couch or on a blanket spread on the floor, clothed simply in his underwear; the hands are placed at the sides. The exercise begins by slowly raising the limbs from the couch to a vertical position in the air, keeping them there for thirty seconds, then very slowly letting them return to the horizontal position of rest. The secret of this manoeuver is its slow execution. With one hand on the abdominal muscles, the patient may feel the tightening and rigidity that occur in the act of raising the limbs. This exercise should be repeated ten times. No. 2 . — The second exercise should be carried out in the follow- ing manner : The patient places himself flat on a blanket on the floor, with his feet inserted under a bureau or under a piece of heavy furniture of any kind ; both hands are placed at the sides. The patient now must slowly bring the trunk of his body into an TREATMENT OF GASTROPTOSIS. 727 erect position, and when this has been reached, the trunk is just as slowly replaced in a prone position on the floor. Both of these exercises are quite similar; in No. i it is the trunk which is fixed and the lower limbs are slowly moved up and down, and in No. 2 the lower limbs are fixed and the trunk is moved up and down. These exercises should be carried out systematically and methodically ten times every morning and evening. Sandow’s book on training will instruct those desiring information on this very useful subject. Rapid emaciation must be avoided. Physicians are nowadays frequently consulted by thin people desiring to get fat, and by fat people desiring to become thin, in the most convenient manner. Rapid falling-off and loss of fat, when undertaken as a cure for obesity, is a hazardous undertaking. The fat is lost not only from the trunk and extremities, but the internal organs are deprived of their normal incasing and imbedding of fat, which constitutes their support, so that treatments tending to reduce the weight of the body should be conducted only under careful supervision. The Mechanical Treatment . — The mechanical treatment consists in applying a properly selected and adapted abdominal bandage. There is no one particular bandage that will suit all cases. The bandages should have their main support and resting-places upon the crests of the ilium, symphysis pubis, and spinal column. From here the strength of the bandage is secured by broad pieces of metal or whalebone inserted into the linen, leather, or rubber parts of the bandage. These bandages must be measured to the nude figure, must fit perfectly, and should be worn day and night. Boas recommends the bandage of Landau and Bardenheuer. Prolonged rest in a horizontal position on the back favors restitution of the abdominal viscera to their normal position. In cases of great weakness, therefore, with emaciation, the Weir Mitchell rest cure is one of the most effective means of treatment. Constipation is best combated by proper diet. The author recom- mends compotes of fruit, such as figs, prunes, apples, pears, plums, and sweet grapes. Buttermilk, kefyr, and good cider favor normal evacuation. Sugar of milk, y 2 of an ounce three times daily, is also helpful. The injection of eight ounces of olive oil high up into the colon is an excellent treatment for this symptom (Fleiner). As gastroptosis predisposes to dilation, it may occur that the foods are retained an abnormally long time within the stomach. In these cases lavage will be indispensable. 728 ENTEROPTOSIS GASTROPTOSIS. When the symptoms of atony and motor insufficiency are pro- nounced, local intragastric douches with alternating cold and warm water are very effective in restoring partial tonicity to the muscular walls. Turck’s gastric resuscitator is available for this purpose. The temperature of the water should be changed every two or three minutes by alternately connecting the stomach-tube with hot and cold reservoir-bottles, elevated to about the level of the patient’s head. The tube is of the return or double-current type, and the water does not come in contact with the mucosa, but flows through a rubber bag which distends the stomach moderately. (See Gillespie, “ Modern Gastric Methods,” p. 164.) Treating the abdominal muscles by massage and the faradic current is of some utility in patients that are too feeble to undergo the abdominal gym- nastic training. These means of treatment may be applied also in those cases that have not the will-power to persist in such abdominal gymnastics; but electricity and massage can not effect the per- manent improvement that results from abdominal gymnastics. Floating kidneys, according to Bachmeier (“ Wien. med. Presse,” 1891, Nos. 19 and 20), may be replaced best in the following manner : The patient occupies the dorsal position in bed, the physician taking a chair facing the head end of the bed ; both hands are placed on the right side of the patient, under the anterior arch of the ribs ; if possible, the kidney is grasped with the fingers of the right hand ; the hands are then pressed gently and firmly toward the posterior and superior parts of the abdomen. While this pressure i^ exerted, the finger-tips must make constant shaking and trembling motions. The author prefers placing the patient in a recumbent dorsal position with the pelvis very much elevated and the chest and head low; for example, the patient may sit upon the high part or head-rest of a sofa, and let the body sink slowly down backward upon the couch ; the dislocated kidney will then of itself resume its normal location, — provided it is not adherent, — particularly if the manipulations just described are carried on at the same time. Diet . — In enteroptosis and gastroptosis the diet should be as nourishing as possible, and adapted to the state of motility and secretion. If the condition of the digestive organs will permit, attempts should be made at increasing the adipose tissue. Distinct diseases of the gastric mucosa contraindicate a large food-supply. Experience has taught us that one of the best treatments for float- ing kidney is that which causes an increased deposition of fat. MEDICINAL TREATMENT. 729 Fat is best introduced in diet in the form of fresh butter, rich gravies, and cream. For further particulars of nourishing diet we refer to the section on Dietetics. In the author’s sanatorium for digestive diseases the schedule on pages 249 and 250 has been found useful in nephroptosis. In a number of cases where fats in the diet gave digestive distress, I succeeded in increasing the body weight by hypodermic injections of sterile olive oil. Medicinal Treatment. — The' use of medicines is sometimes una- voidable for the treatment of constipation. My favorite remedy for this, when it becomes necessary, is the fluid extract and the active syrup of cascara sagrada (Clinton Pharm. Co.), or large colon irrigations with warm water, which will also benefit the mem- branous colitis. When patients can take it, the time-honored castor oil is a good and harmless remedy, but must not be given when there is gastric stagnation. Of other laxative remedies, I favor aloes, strychnin, rhubarb, magnesia, senna, and podophyllin. Jalap and scammony do not act well, nor do the very drastic pur- gative waters, such as the Hunyadi Janos and Rubinat-Condal. In such rare cases as could tolerate water-drinking I have seen more favorable results follow the persistent use of Bedford Magnesia Springs water, which is rather mild in its purgative qualities. On the whole, I have observed no permanent improvement under the use of any mineral waters. Glenard recommended magnesium and sodium sulphate to com- bat the effects of autointoxication ; but Boas, after a prolonged trial of these remedies, asserts that he has observed detrimental results from them. The author’s formula for combating auto- intoxication in gastroptosis is the following : R. Betanaphthol bismuth, 4.0 Resorcin resublim., 4.0 Strychnin, sulphatis, 0.02 In anacidity (achylia) dilute HC 1 , gvj, should be added Elix. gentianse, 1 80.0 Sig. — O ne tablespoonful three times daily. In addition to these, the salicylate of bismuth, salicylic acid, chloroform water, and betanaphthol have been recommended. They are made more efficacious if combined with strychnin and an adapted diet. It is conceivable that methods of surgical procedure for replac- ing a prolapsed stomach, by attaching it partly to the diaphragm, ensiform cartilage, and perhaps to the retroperitoneal fascia, in ■ Z) 3J gr- A fgvj. M. 730 ENTEROPTOSIS GASTROPTOSIS. such a manner as to avoid kinking or stenosis (gastropexy), may prove practicable. This operation has been recently described in the following publications: Duret, see “ Rev. de Chir.,” 1896, xvi, p.421 ; also Davis, “ Western Med. Rev.,” Oct., 1897, W. W. Keen, “ Cartwright Lectures,” “ Phil. Med. Jour.,” vol. 1, p. 935. LITERATURE ON GASTROPTOSIS AND ENTEROPTOSIS. 1. Aaron, C. D., “ Gastroptosis,” “Jour. Amer. Med. Assoc.,” 1897, xxiv. 2. Adler, H., “Gastroptosis: A Clinical Study,” “Maryland Med. Jour.,” Baltimore, 1898, xxxix. 3. Arendt, “ Ueber Mastcuren und ihre Anwendung bei chronischen Krank- heiten der weiblichen Sexualorgane,” “ Therap. Monatshefte,” 1892, Heft 1, S. 9. 4. v. Bachmaier, “ Die Wanderniere und deren manuelle Behandlung, nach Thure Brandt,” “Wiener med. Presse,” 1892, Nr. 19 u. 20. 5. Bial, M., “Ueber die Beziehung der Gastroptose zu nervosen Magen- leiden,” “ Berl. klin. Wochenschr.,” 1897, xxiv. 6. Bial, M., “ Gastroptose,” “ Verhandl. d. Cong. f. innere Med.,” Wies- baden, 1897, xv. 7. Boas, “ Ueber die Bestimmung der Lage und Grenzen des Magens durch Sondenpalpation,” “ Centralbl. f. klin. Med.,” 1896. 8. Bourget, “Ueber den klinischen Werth des Chemismus des Magens,” “Therap. Monatshefte,” 1895. 9. Chapotot, “ L’Estomac et le Corset,” Paris, 1891. 10. Cheron, “ De l’Enteroptose,” “Union Med.,” 20. Dec., 1888. 11. Cuilleret, “Etude Clinique sur l’Enteroptose ou Maladie de Glenard,” “ Gazette des Hopit.,” 1888, et No. 105, 1889. 12. Czerny, “ Zur Prophylaxis des Hangebauches der Frauen,” “ Centralbl. f. Gynakologie,” 1886. 13. Dehio, “ Zur physikalischen Diagnostik der mechanischen Insufficienz des Magens,” VII. Congress, f. innere Medicin, 1888. 14. Dujardin-Beaumetz, “ Neurasthenie Gastrique et leur Traitement,” “ Lemons de l’Hopital Cochin,” in the “ Therapeut. Gaz.,” 15 Jan., 1890. 15. Edinger, “ Wanderniere,” “ Eulenberg’s Real-Encyklop.,” 2. Aufl.,xxi. 16. Einhorn, M., “Die Gastrodiaphanie,” “ New Yorker med. Wochenschr.,” 1889* 17. Ewald, “Ueber Enteroptose und Wanderniere,” “Berl. klin. Woch- enschr.,” 1890. 18. Fereol, “ De l’Enteroptose,” “ Bulletin de la Societe Med. des Hopitaux,” 5 Janv., 1887, et i2Novembre, 1888. 19. v. Fischer-Benzon, “Ein Beitrag zur Anatomie und Aetiologie der be- weglichen Niere,” Inaug.-Dissert., Kiel, 1887. 20. Fleiner, “Ueber die Behandlung der Constipation und einiger Dick- darm-Affectionen mit grossen Oelklystieren,” “ Berl. klin. Wochenschr.,” 1893. 21. Fleiner, “Ueber die Beziehungen der Form- und Lageveranderungen des Magens und des Dickdarms zu Functionsstorungen und Erkrankungen dieser Organe,” “ Miinch. med. Wochenschr.,” 1895. 22. Fromont, “ Anatqmie de la Portion Abdominale de l’lntestin,” These de Lille, 1890. 23. Gegenbaur, “ Lehrbuch der Anatomie des Menschen.” LITERATURE ON GASTROPTOSIS AND ENTEROPTOSIS. 731 24. Glenard, “Application de la Methode Naturelle al’Analyse de la Dys- pepsie Nerveuse,” “ Lyon Med.,” 1885 ; “ Enteroptose et Neurasthenic,” Soc. Medic, des Hop. de Paris, 1886; “ Expos6 Sommaire du Traitement de l’Ent6- roptose,” “ Lyon Med.,” 1887, etc. 25. Glenard, “ De l’Enteroptose, conference facite a l’hopital de Mustapha,” Alger-Lyon, Janv., 1889, “ Presse med. Belg.,” Bruxelles, 1889. 26. Hahn, “Operative Behandlung der beweglichen Niere durch Fixation,” “ Centralbl. f. Chirurgie,” 1881, No. 29 (Nephrorrhaphy). 27. Hasse, “ Bewegung. d. Zwerchfells — Einfluss derselben auf d. Unter- leibsorgane,” “ Archiv f. Anat. und Physiol.,” 1886, S. 185. 28. Hertz, P., “ Abnormitaten in der Lage und Form der Bauchorgane bei dem erwachsenen Weibe,” Berlin, 1894. 29. Hilbert, “ Ueber palpable und bewegliche Nieren,” “ Deutsches Archiv f. klin. Med.,” 1893, Bd. l. 30. Huber, A., “ Beitrag zur Kenntniss der Enteroptose,” Sonderabdr. a. d. “ Correspondenzbl. f. Schweizer Aerzte,” 1895, Nr. 11. 31. Hufschmidt, “ Pathol, und Therap. d. Enteroptose,” “ Wien. klin. Wochenschr.,” 1892, Nr. 52, including Literature. 32. Israel, “Ueber die Palpation gesunder und kranker Nieren,” “ Berl. klin. Wochenschr.,” 1889. 33. Kelling, “ Ein einfaches Verfahren zur Bestimmung der Magengrosse mittelst Luft,” “ Deutsche med. Wochenschr.,” 1892. 34. Kelling, “ Physikalische Untersuchungen liber die Druckverhaltnisse in der Bauchhohle, sowie liber die Vitalcapacitat des Magens,” Leipzig, 1896. 35. Keppler, “ Die Wanderniere und ihre chirurgische Behandlung,” Ber- lin, 1879. 36. Knapp, Ludwig, “ Wanderniere bei Frauen,” Monograph (Report from Rosthorn’s Clinic in Prague), Berlin, 1896. 37. Konig, G., “ Chemische Zusammensetzung der menschlichen Nah- rungs- und Genussmittel,” Berlin, 1889 und 1893. 38. Krez, L., “ Zur Frage der Enteroptose,” “ Mlinch. med. Wochenschr.,” No. 35, 1892. 39. Kumpf, “ Ueber die Wanderniere der Frauen und deren Behandlung,” “ Wiener med. Blatter,” 1890, Nr. 14. 40. Kussmaul, “ Die peristaltische Unruhe des Magens, nebst Bemerkungen iiber Tiefstand und Erweiterungen desselben,” etc., “ Volkmann’s Sammlung klin. Vortrage,” Nr. 181. 41. Kuttner, “Ueber palpable Nieren,” “Berl. klin. Wochenschr.,” 1890. 42. Kuttner, “ Einige Bemerkungen zur elektrischen Durchleuchtung des Magens,” “ Berl. klin. Wochenschr.,” 1895. 43. Kuttner, L., und Dyer, “ Ueber Gastroptose,” “ Berl. klin. Wochenschr.,” 1897, XXIV. 44. Landau, “ Die Wanderniere der Frauen,” Berlin, 1881. 45. Leo, “ Diagnostik der Krankheiten der Bauchorgane,” 2. Aufl., 1895. 46. Leube, “ Specielle Diagnostik innerer Krankheiten,” 1891. 47. Lindner, “Ueber die Wanderniere der Frauen,” Neuwied, 1888. 48. Litten, “ Ueber den Zusammenhang der Magenerkrankungen mit Lage- veranderungen der rechten Niere,” “ Verhandl. des Congresses f. innere Medicin,” vi, 1897; ferner : Berl. med. Gesellschaft, Sitzung vom 19. Marz, 1890; “ Berl. klin. Wochenschr.,” 1890, Nr. 15. 732 ENTEROPTOSIS GASTROPTOSIS. 49. Luschka, “ Lage der Bauchorgane,” Atlas, Karlsruhe, 1873. 50. Malbranc, “ Ein complicirter Fall von Magenerweiterung,” “ Berl. klin. Wochenschr.,” 1880, No. 28. 51. Martius, “ Ueber Grosse, Lage, und Beweglichkeit des gesunden und kranken Magens,” “ Verhandlungen der LX VI. Naturforscherversammlung,” 1894. 52. Meinert, E., “Ueber einen bei gewohnlicher Chlorose des Entwickelungs- alters auscheinend konstanten Befund,” etc., “Volkmann’s Samml. klin. Vortrage,” 1895, Nr. 115 u. 116. 53. Meinert, E., “ Zur diagnostischen Verwerthbarkeit der Magendurch- leuchtung,” “ Centralbl. f. klin. Med.,” 1895. 54. Meinert, E., “Ueber normale und pathologische Lage des menschlichen Magens und ihren Nachweis,” “Centralbl. f. innere Med.,” 1896. 55. Meinert, E., “Zur Aetiologie der Chlorose,” Wiesbaden, 1894. 56. Meltzing, “ Magendurchleuchtungen,” “ Zeitschr. f. klin. Med.,” XXVII. 57. Meltzing, “ Gastroptose und Chlorose,” “ Wiener med. Presse,” 1895. 58. Moritz, “ Studien iiber die motorischeThatigkeit des Magens,” “ Zeitschr. f. Biologie,” xxxii, Neue Folge, xiv. 59. Muller-Warneck, “Ueber die widernatiirliche Beweglichkeit der rechten Niere,” “ Berl. klin. Wochenschr.,” 1877. 60. Munk und Uffelmann, “ Die Ernahrung des gesunden und kranken Menschen,” 2. Aufl., Wien und Leipzig, 1891. 61. Oser, “Die Ursachen der Magenerweiterung,” “Wiener Klinik,” Januar, 1881. 62. Pick, A., “Magen- und Darmkrankheit,” Wien, 1895, pp. 179-188 (35 bibliographical references). 63. Pourcelot, “ De l’Enteroptose,” “ Union Med.,” 20'Dec., 1888. 64. Putnam, J. J., “ Case of Splanchnoptosis and Achylia Gastrica with Mel- ancholia,” “ Boston Med. and Surg. Jour.,” Nov. 17, 1898. 65. Reichmann und Heryng, “Ueber elektrische Magen- und Darmdurch- leuchtung,” “ Therap. Monatshefte,” 1892, S. 128. 66. Riegel, “ Die Erkrankungen des Magens,” Wien, 1896. 67. Runeberg, “ Ueber die kiinstliche Aufblahung des Magens und des Dickdarms durch Luft,” “ Deutsch. Archiv f. klin. Med.,” 1884, Bd. xxxiv. 68. Schultz, E., “Wanderniere und Magenerweiterung,” “ Prager med. Wochenschr.,” 14. Januar, 1885. 69. Stiller, B., “Enteroptoseim Lichte eines neuen Stigma neurasthenicum,” “Archiv f. Verdauungskrankh.,” Bd. II, S. 285. 70. Sulzer, M., “Ueber Wanderniere und deren Behandlung durch Neph- rorrhagie,” “ Deutsche Zeitschr. f. Chirurgie,” 1891, Bd. xxx, S. 506. (This article contains the complete literature on the Pathology and Treatment of Floating Kidney up to that date.) 71. Trastour, “ Les Desequilibres du Ventre, Enteroptosiques et Dilates,” “ Semaine Medic.,” 7 Sept., 1887. 72. Volcker, “ Die Schadlichkeit des Schniirens,” Dissert., Miinchen, 1893. 73. Weil, “ Handbuch und Atlas der topographischen Percussion,” Leipzig, 1880. 74. Weisker, Cl., “Ueber den sog. intra-abdominellen Druck,” “Schmidt’s Jahrbiicher der gesammten Medicin,” Bd. ccxix, S. 227. NEUROSES OF THE STOMACH. 733 CHAPTER X. NEUROSES OF THE STOMACH. Gastric neuroses may be classified as follows : I. Motor. II. Sensory. III. Secretory. Under each one of these we may distinguish — (a) States of excitation. ( b ) States of depression of nervous influences. I. Neuroses of Motility, or Peristalsis. (a) Irritative states : (1) Cramp of the cardia, or cardiospasm. (2) Cramp of the pylorus, or pyloric spasm. (3) Cramp of the entire musculature, or gastrospasm. (4) The peristaltic unrest of Kussmaul. (5) Nervous eructation. (6) Nervous vomiting. (b) Depressive states : (1) Insufficiency of the cardia, including rumination and regurgitation. (2) Insufficiency or incontinence of the pylorus. (3) Atony or insufficiency of the entire gastric musculature (gastroplegia). II. Sensory Neuroses. (a) Irritative states : (1) Hyperesthesia. (2) Gastralgia. (3) Bulimia and polyphagia. {b) Depressive states : (1) Acoria. (2) Anorexia. III. Neuroses of Secretion. (a) Irritative states : (1) Hyperchylia, hyper- or superacidity. (2) Supersecretion or gastrosuccorrhea, gastroxynsis. (b) Depressive states : (1) Hypochylia or subacidity. (2) Achylia gastrica and anacidity. Nervous Dyspepsia. Neurasthenia Gastrica. 734 NEUROSES OF THE STOMACH. General Considerations. — All diseases of the stomach in which no pathological anatomical change can be demonstrated in the organ are classed as neuroses. Hitherto we have considered only diseases that were based upon an actual alteration in the structure of the stomach. Neuroses, then, are idiopathic diseases of the gastric nerves, with absence of histological changes that can be demonstrated in the tissues. The gastric nerves can be affected, it is true, in the course of gastritis, ulcer, carcinoma, and dilation, by the changes in the deeper layers of the stomach brought about by these diseases. A large portion of the dyspeptic disturb- ances, as well as of the anomalies of secretion and motility, are attributable to injurious influences exerted upon the nerves in the course of these diseases. These nervous affections which accom- pany changes in the gastric structure are known as secondary symptomatic nervous disturbances. It is very probable that ana- tomical changes may lie at the foundation of many neuroses, but up to the present time they escape our microscopical technic. For instance, in more than half the cases of hyperacidity a proliferation of the oxyntic cells, or of the gland tubules as a whole, has been ascertained by Hayem, Einhorn, Cohnheim, and myself (Hem- meter, “ Histologie d. Magendriisen bei Hyperaciditat,” “Archiv f. Verdauungskrankh.,” Bd. iv, S. 23). It is more than probable, also, that atrophy is present in from one-half to two-thirds of the cases of achylia gastrica. With further progress and improvement of our methods of staining and hardening the number of gastric neuroses will become more and more reduced. The histological changes in the mucosa accompanying hyper- chylia and achylia are not caused by the nervous condition, but constitute a primary affection independent of the neurosis. This is made probable by the fact that proliferation of oxyntic cells and of gland tubules can be found at the autopsy, in the stomachs of individuals who have never shown any symptoms of nervous dis- eases or neurasthenia, and also because proliferation has been found in fragments of mucosa gained from the wash-water of perfectly normal individuals so far as any neuropathic state was concerned. When the gastric nervous apparatus is the primary seat of the disease, it is called a primary neurosis, but when the disease of the gastric nerves is reflexly excited from the central nervous system, or from other organs, such as the intestines, liver, spleen, and kid- neys, it is called a secondary or reflex neurosis. Neuroses may N EUROS ES OF THE STOMACH. 735 cause secondary anatomical alterations in the stomach — for in- stance, if anacidity is associated with impaired motility, we may have a gastritis develop from decomposition of a stagnating ingesta. When hyperacidity, or supersecretion, causes a persistent spasm of the pylorus, a dilation may result producing the same symp- toms. Disturbances of the sensory nerves of the stomach may extend to the bowels, and bring about the so-called neurasthenia or nervous dyspepsia of the intestines ; with persistent nervous atony of the stomach the motility of the intestine frequently begins to suffer also. This, apparently, is a direct extension of the ner- vous trouble to the intestines. In achylia gastrica, when the anti- septic effect of HC1 is missing, an excessive putrefaction of the intestinal contents with abundant formation of gases is sometimes noticed, so that the intestinal wall becomes very much expanded, and an atony can arise in this manner. It is well known that strong psychic impressions and emotions like anger, aggravation, fright, fear, and sadness, as well as excessive joy, can completely suppress the appetite. In very excitable people these emotions may even cause eructation, nausea, and severe gastralgia. These nervous disturbances mend rapidly, as a rule, when the mind has been quieted; but when the emotional excitement was great, and frequently repeated within a short time, particularly in very excitable, neuropathic individuals, a lasting neurosis may de- velop. Gastric neuroses which are the result of functional or anatomical diseases of the nervous central organs, of hysteria and neuras- thenia, may be so prominent that the fundamental disease may be completely submerged, and be little regarded by the patient, and is not discovered by the physician until after a careful study of the case has been made. In sclerosis of the posterior columns of the spinal cord (tabes dorsalis) a train of gastric symptoms has been first described by Charcot under the name of “ crises gastriques.” They are described as intense cramp-like pains occurring suddenly in the midst of comparative well-being, and radiating toward the abdomen and back ; they are usually followed by copious vomiting. The vomit at first consists of food, and later of mucus, bile, and duodenal secretions, and may occur several times in the same day, frequently every hour. These attacks appear and disappear very rapidly, and are separated by long intervals of perfect freedom .from gastric disturbances. Ewald emphasizes that these attacks may occur in tabes so early in the disease that the fundamental 736 GASTRIC NEUROSES. affection can not in all be diagnosed because all typical symptoms are wanting. Sensations of a boring and burning character and severe gastralgia may be present in tabic patients years before the spinal disease is recognizable (Seymour Basch, “ Arch. f. Verdau- ungskr.,” Bd. v, 1899). In other anatomical diseases of the nervous central organs, in myelitis due to compression, meningitis, brain tumors, and after powerful concussions of the brain and spinal cord, nervous gastric disturbances appear. In the progress of certain dis- eases of the medulla, repeated nausea and vomiting may be attributed to irritation of the vomiting center. Reflex neuroses of the stom- ach may occur from disease of the neighboring organs : as, for instance, from the liver, intestines, bile passages, spleen, and periton- eum, as well as from the kidneys, sexual organs, and heart. In biliary colic gastric symptoms are rarely absent. We generally find that gastralgia, nausea, vomiting, eructation, and anorexia are present during the passage of gall-stones, and rapidly disappear as soon as the stone has passed through into the intestine. The gastric complications of cholemia and cholelithiasis do not disappear so rapidly, because the excretion of the foreign materials in the blood of cholemia, and the correction of anatomical changes in chole- lithiasis require time. Renal colic in a similar manner may cause dyspeptic symptoms. Cases are reported in which the renal symp- toms were so masked by the gastric that the diagnosis of peptic ulcer was made. This may very readily occur when the nephritic pains radiate toward the back and shoulders like those of ulcers. Gastric symptoms occurring as a sequence to uremia are the result of a direct or indirect irritation of the central nervous organs, and also of the gastric nerves by retained products of catabolism. In cases of contracted kidney with chronic uremia in my clinic the patient suffered exclusively from gastric symptoms, but test-meals showed that the motor and secretory functions were normal, at times at least, and that, therefore, the dyspeptic complaints were disturb- ances of the sensory nerves of the stomach. Diseases of the sexual organs, in both sexes, but particularly in women, may bring about reflex gastric neurosis. Kretschy and Fleischer have found that the physiological process of menstruation may cause disturbances of gastric function, which naturally are also met with in a more exaggerated form in dysmenorrhea, in diseases of the uterus and ovaries, and during pregnancy. Whatever may be the etio- logical culmination of factors in vomiting of pregnancy , there is no better explanation offered up to the. present time than that it is a ANATOMY AND PHYSIOLOGY OF GASTRIC NERVES. 737 reflex neurosis of the stomach induced by the expansion of the uterus and irritation of the sympathetic fibers caused thereby. R. Frommel (Penzoldt and Stintzing’s “ Handbuch d. specielle Therap. innerer Krankheiten,” Bd. iv, S. 440) has obtained very good results in this disease with basic orexin, a medicine which acts mainly in nervous affections, and rarely in anatomical alterations of the stomach. Gastric neuroses are much more frequently seen in women than in men. Women and girls of the better classes constitute the pre- vailing number of those affected with gastric neuroses. The recog- nition of pure gastric neuroses and whether they exist as idiopathic independent diseases, or are in some causal relation to a preexist- ing disease, like those we have mentioned, is often a problem presenting great difficulties. The stomach is an organ that is very rich in nerves, and is inclosed in a widely connected net- work of fibers which bring it into close connection with other vital organs. ANATOMY AND PHYSIOLOGY OF GASTRIC NERVES. Concerning the anatomy and physiology of the gastric nerves, we may say that the innervation of the organ is carried out above all by the vagi. The left vagus spreads over the cardiac portion and the lesser curvature, and forms the anterior gastric plexus with fibers coming from the abdominal sympathetic. The right vagus supplies mainly the liver, pancreas, spleen, kidney, and small intestine, and a small part of its branches reaches the posterior wall of the stomach. Anastomoses from the abdominal sympa- thetic with branches of the right vagus form the posterior gastric plexus. The vagi also enter into the formation of the celiac or solar plexus. Branches from the solar plexus form the so-called superior coronary plexus of the stomach lying along the lesser curvature, while branches coming from the hepatic plexus and running along with the right inferior coronary artery form the inferior coronary plexus of the stomach. These four plexuses are united into a great network by connecting communicative branches. In the pyloric portion, the beginnings of the large and important intestinal plexuses can be demonstrated. The intestinal sympa- thetic nerves form a network with close meshes in the submucosa as well as in the muscular layer. In the broadened points of union of this nervous network are found numerous ganglion cells. The 738 NEUROSES OF THE STOMACH. Meissner network supplies the muscularis mucosae, and the mucosa and the intermuscular plexus of Auerbach supply the muscular layers with very fine branches. Openchowsky has demonstrated large masses of ganglion cells not only at the pylorus, but all along the fundus and cardia m the serosa ; these ganglia are in communication with the large vagosympathetic fibers. Our knowledge of the physiology of the gastric nerves is, up to the present time, very limited. Since the publication of the first edition, Pawlow has repeated and published his work on gastric innervation and secretion (“ Die Arbeit d. Verdauungs- driisen,” S. 71), which proves beyond a doubt that the vagus is the secretory nerve of the gastric glands. The influence of the vagus and sympathetic fibers on peristalsis is but imperfectly understood. Although we do not know the exact paths of vast secretory motor and absorptive impulses, nor of sensation, it is generally assumed on clinical grounds that each of these functions is represented by different nerves, and we therefore accept the exist- ence of special nerves for motion, sensation, secretion, and absorp- tion. Clinical experience has confirmed this assumption because peristaltic, sensory, and secretive disturbances may exist by them- selves. All gastric neuroses may show considerable variation in their course. Thus, the contents of the stomach may one day show anacidity or achylia, and on the next day show hyperchylia. In the same manner we may find motor insufficiency alternating with peristaltic unrest. Although the neuroses may exist singly as in- dividual diseases, we are confronted, as a rule, with combinations of various disturbances. Thus, we may find that hyperacidity and gastrospasm are associated with each other, that hyperesthesia will be combined with vomiting, and that supersecretion may be present in atony. These diseases may develop pronounced attacks at periods when the stomach is resting. The intensity of the attack is very frequently entirely independent of the quantity or quality of the food, but the effect of psychic influences is generally unmis- takable. Neuroses may exist side by side with organic diseases of the stomach, but, as a rule, they are part of the symptomatology of neurasthenia or hysteria. The symptoms of a general neurosis are rarely absent : that is, the characteristic changes of the psychic indisposition, the lassitude, irritability, feeble memory, indisposition to work, insomnia, neuralgia, migraine, vertigo, polyuria, weakness CARDIOSPASM. 739 of the bladder, and a varying pain. All these neuroses which we have mentioned are really not individual diseases, but rather symp- toms; but, as these symptoms generally occur with a certain inde- pendence and are disturbances peculiar to themselves, it will not be illogical to call -the complex anomalies by the name of one symptom, so that we will speak of cardiac spasm and nervous eructation and hyperacidity as diseases peculiar to themselves, bearing in mind, however, that we are simply describing symptoms. CARDIOSPASM (Cramp of the Cardia). The etiology of spasm of the ring musculature of the cardia agrees fully with that of cramp of the pylorus. In the great majority of cases the cramp of the cardia represents a secondary disease, which may appear with hyperesthesia and very strong irri- tation of the mucous membrane of the cardiac region ; further, with abnormal dilation of the stomach through air and gases, as well as with caustic action upon the mucous membrane present with ulcer and ulcerating carcinoma of the cardia ; hence, it is produced by the same causes as cramp of the pylorus. Much more rarely the spasm of the cardia is due to a genuine symptomatic or idiopathic neurosis of the motor apparatus, which is characterized by an increased irritability. It is observed as a symptom of hysteria and neurasthenia, simultaneous with other nervous disturbances, which may facilitate the recognition of the neuropathic basis of this form of cramp. Whether cramp of the cardia as a pure neurosis of the motor apparatus is a functional impairment of the periph- eral motor-nerve apparatus, or whether it is of central origin, is at present still a debated question. We may distinguish two forms of cramp of the cardia : 1. Acute cramp, which, appearing rather suddenly, often spas- modically, is generally only of short duration. 2. Chronic cramp, which is a very stubborn and serious dis- ease. One of the most frequent causes of the rare form of secondary cramp is dilation of the stomach by air and gases. An abnormal dilation of the stomach by air, which may finally bring about a cramp of the cardia, is found mostly in those persons who have the nervous habit of swallowing large quantities of air. If the air is not soon removed through eructation, it keeps on collecting in the stomach and expands on becoming warmed, so that finally a 740 NATURE OF CARDIOSPASM. considerable dilation of the stomach is produced, and with it cramp of the cardia, which is, perhaps, always complicated with cramp of the pylorus. Ewald and Fleischer have had oppor- tunity to examine, repeatedly, cases of intentional swallowing of air. Fleischer’s case was a girl who had been practising it as a kind of sport for many years. The stomach was constantly dilated, even in a jejune state, and felt like an air-pillow. The rounding of the region of the stomach was plainly visible, even through the cloth- ing. The elastic stomach-tube introduced into the esophagus met an obstruction at the cardia, which was not easily overcome, even after the insertion of the tube into the stomach. When the outer end was put into water, numerous bubbles of air escaped through it; but even with a strong external pressure in the region of the stomach one could not succeed in removing all the air. The re- sistance in this region continued, though to a less degree. With repeated thorough palpation it was discovered that the cramp of the cardia and pylorus, occurring intermittently for many years, had caused a hypertrophy of the musculature of the stomach; and it was this condition, probably, which prevented the formation of a more severe atony and ectasia of the stomach, for the lower limit of the stomach was only slightly below the normal. The stomach may also be dilated by a very copious intragastric formation of gases to such a degree that a cramp of the cardia arises ; and this happens very easily when the formation of gases is very rapid, as is observed sometimes with protracted stagnation of the ingesta in the stomach, as a result of atony, ectasia, chronic gastritis, advanced stenosis of the pylorus or duodenum, as well as with primary and secondary cramp of the pylorus, when the contents of the stomach are subject to fermentation and decom- position. If the gases can not pass over into the intestine, they continue to collect in the stomach, which finally becomes very much dilated; the region of the stomach becomes arched, and troublesome sensations of pressure and tension appear in the same. If the stomach presses the diaphragm upward, and if the latter in turn presses on the lower part of the lung and the heart, dyspnea, precordial oppression, palpitation of the heart, and “ asthma dyspepticum ” may result. With this there sometimes exist great prostration, rapid, soft pulse, and headache. That these very often dangerous symptoms are really caused by the dilation of the stomach and not, perhaps, by autointoxication, — that is, by toxic products of fermentation and putrefaction of the chyme, — is SYMPTOMS AND COMPLICATIONS OF CARDIOSPASM. 74 1 evident from the fact that the symptoms cease quickly when the cardiac closure is finally broken (the pylorus, on account of its very n\uch stronger ring musculature, offers a much greater resist- ance to the passage of the gases into the intestines), when the spasm relaxes, or a ‘tube is introduced into the stomach, and the air or gases have an opportunity to escape outwardly. Very rapid distention of the stomach with air pumped in through the tube or evolved from bicarbonate of sodium by tartaric acid may bring on cardiospasm of a short and transient nature. In highly neurotic patients distention should be carried out very slowly. On the other hand, the cramp of the cardia may also be primary, and the dilation of the stomach (pneumatosis) may be secondary. If the cramp of the cardia sets in immediately after the meal, and if the eructation of the air which is swallowed during the meal with the food and liquids is prevented, then the stomach may also become abnormally distended. Since the neuromuscular apparatus of the cardia is mechanically irritated with strong distention of the stomach, the cramp is prolonged thereby, and, therefore, it probably lasts longer during digestion than with an empty stomach. Just as the removal of air and gases from the stomach through eructation is sometimes made entirely impossible by a primary or secondary cramp of the cardia, so the removal of the contents of the stomach by vomiting may also be made impos- sible. Even the strongest efforts at vomiting bring up nothing, and patients may be much tormented by fruitless muscular exertion. When this is of long duration and frequent repetition, it may bring about atony of the stomach in consequence of over- exertion of the musculature. If the cramp is caused as a second- ary or reflex neurosis by hyperesthesia, strong irritation, or ulceration of the mucous membrane of the cardia, it sometimes produces a painful feeling of contraction in the region of the cardia, which may radiate toward the breast, the back, and to the region of the heart. It has been asserted that the cramp which appears as a pure neurosis of the motor apparatus may also cause the same sensations of pain, but this is not very probable. At least my observations with that form of cramp of the pylorus that is not dependent upon the states of disease before mentioned, but de- pends simply upon a pure neurosis of the motor apparatus, argue against it, since the latter is not accompanied by pain. The pains described are not a constant symptom, and, therefore, may not be used as a factor in a differential diagnosis of the two forms of cramp. 49 742 SYMPTOMS AND PROGNOSIS OF CARDIOSPASM. Since with an entirely empty stomach the acute spasm produces no symptoms, it may remain latent for some time, and is sometimes recognized only by accident, when for some reason a tube is introduced into the stomach which meets an obstruction in the region of the cardia, or when food or drink is taken by the pa- tient during the cramp, deglutition being then impeded. Chronic cardiospasm gives much more significant symptoms. Besides the symptoms mentioned previously, very severe complaints from deglutition appear. The patients have the unmistakable feeling that some of the food becomes stuck before it reaches the stomach. If, in spite of this, the meal is continued, the lower part of the esophagus is filled with food, which after some time the patients, with great exertion, succeed in bringing up again in an almost unchanged condition. That it comes from the esophagus and not from the stomach is shown by the absence of the free hydrochloric acid. The second deglutition sound (auscultation over the lower part of the sternum) is always lacking, and in its place a low, rippling noise may be heard, which probably arises from the circumstance that the cardia is not completely closed, and liquids pressed on may still flow into the stomach. With protracted duration of the malady, the ingesta remaining in the lower part of the esophagus may exert such a pressure upon its walls that a diverticulum may be formed, which prevents the taking in of food. The nutrition of patients may be much reduced, so that, especially when the patients are advanced in age, the suspicion may arise that a carcinoma of the cardia is developing, which, as we know, can also cause a stenosis of the cardia as well as the formation of a diverticulum. Fortunately, chronic cramp of the cardia is a very rare malady ; it may exist for months, even years. Prognosis. — The prognosis of the acute primary or secondary cramp of the cardia is, on the whole, favorable, especially when it is recognized in time, and if one is successful in rapidly removing its fundamental causes — swallowing of air, formation of gases in the stomach, hyperacidity, hypersecretion, atony, hyperesthesia, etc. The prognosis is always to be made with caution when a diver- ticulum of the esophagus which hinders the passage of food has already been formed. Diagnosis. — In order to distinguish acute primary and second- ary cramp, one must learn, above all, whether one of the diseases before mentioned, which can produce cramp of the cardia, is DIAGNOSIS OF CARDIOSPASM. 743 present. With repeated thorough investigations one generally succeeds in determining the cause of the secondary cramp. If it is due to hyperesthesia, to a strong irritation, or to loss of substance of the mucous membrane of the cardia, then pains in the region of the cardia often draw attention to this manner of origin, and the introduction of a tube into the stomach will then cause pain also. But if a decided cause for the cramp can not be discovered, if it recurs periodically, if it is always of rather short duration, and if other nervous troubles are present, then probably a symptomatic functional neurosis exists; and if all these signs are lacking, then there is an idiopathic functional motor neurosis; but this is a very rare occurrence. The diagnosis of the chronic cardiospasm leading to a perma- nent closure of the cardia is more difficult, because it may easily be mistaken for carcinoma or malignant stenosis of the cardia, as well as for a diverticulum of the lowest part of the esophagus, which, however, is rare. Advanced age, anemia, and cachexia, appearing at a time in which the passage of food is not yet hindered to a great extent, argue for carcinoma of the cardia. In the food brought up by regurgitation, as well as in the examination with the tube, one often finds traces of blood, and in some few cases particles of car- cinomatous structure (in the aperture of the tube). In most of the patients free hydrochloric acid is wanting in the contents or food that may be drawn from the esophageal diverticulum. The more the stenosis increases with the progress of the carcinoma, the thinner the tubes that must be used in order to pass. Cicatricial stenosis of the cardia is less frequent, a diverticulum of the lowest section of the esophagus much rarer, than carcinoma of the cardia. Both diseases are not connected with any particular age. The nutrition of the patients is decreased only when the pas- sage of the food is very much impeded. In the formation of diver- ticulum traces of blood in the contents of the tube are generally lacking, and with cicatricial stenosis they are very rare. With diver- ticulum, tubes of different thicknesses sometimes penetrate into the stomach at the first attempt, at other times only after many fruit- less endeavors, according as the stomach is full or empty. With stenosis, when there is much difficulty in deglutition, only thin tubes can penetrate. In both maladies there are no anomalies of secretion in the stomach. With carcinoma, as well as with stenosis of the cardia and with diverticulum, the difficulties of deglutition 744 CARDIOSPASM. increase very gradually, while in the case of cramp they generally come to an acute stage in a short time. The chronic cramp, which is very rare, may appear at any age. The general nutrition suffers only after protracted duration. Traces of blood can neither be found in the examination with the tube nor in the food that is eructated. The examination of the contents of the stomach in cases of sim- ple cramp of the cardia shows nothing abnormal. With intermit- tent relaxation of the cramp, the difficulties of deglutition cease tem- porarily, and a rigid tube may be pushed into the stomach without meeting with any resistance; neither of these phenomena are ob- served with carcinoma and stenosis, except in the rare case of disin- tegration of the carcinoma. An important distinction of the cramp consists in the fact that thick, rigid tubes overcome the obstacle at the entrance of the stomach much more easily than thin tubes. The same observations have been made repeatedly with spastic stricture of the urethra, which is generally a result of hyperes- thesia of the mucous membrane of the urethra. If in this case a thin catheter is introduced, its point, with moderate pressure, irritates only one spot of the mucous membrane, and by this a cramp of the musculature is produced (or a previously existing one is increased), which becomes so severe that it may easily be mis- taken for an organic stricture. A wrong diagnosis is, however, easily avoided if the mucous membrane is first anesthetized with a four per cent, solution of cocain. Then, after a short time, one can push the catheter further. If a much thicker catheter is introduced, the broader point of the same will exert an even pres- sure upon the whole mucous membrane at the point in question, which is not so irritating. Probably the sensory nerves are then for a time paralyzed, and the cramp abates. Very likely the same conditions obtain in the probing of the esophagus. If after protracted duration of a cramp, a diverticulum of the esophagus has been formed, considerable quantities of food may be retched up at one time, and a thick tube will then pass the obstacle at the entrance of the stomach, the facility of the passage depending on the fullness of the diverticulum, and sometimes the passage is ac- complished only after many unsuccessful endeavors. In all cases when there is any doubt about the differential diag- nosis between cardiospasm and carcinoma of the cardia, the patient should be examined under anesthesia. If the passage becomes readily permeable to the sound under narcosis, carcinoma can be excluded. TREATMENT OF CARDIOSPASM. 745 Among the severest cases of this type occurring in my experi- ence was that of a girl ten years old. The diagnosis was difficult — it could not be decided whether it was a diverticulum, a cicatri- cial stenosis, or cardiospasm. For two weeks the tube inevitably became caught above the cardia. Eventually, I succeeded in passing a tube under anesthesia, and thereafter the intubation became less difficult of execution even while the patient was conscious. For a month previous to consulting me the child could not swallow any solid food, which had resulted in extreme emaciation. After three intubations under anesthesia she began to swallow semisolid food material, and she was ultimately cured by electricity and daily passage of the tube. Naturally, the inspection of the esophagus with the esophago- scope would decide most of such cases. (See p. 183.) Therapeutics. — The patient must abstain from all injurious influences. The abnormal conditions which, according to experi- ence, produce cramp of the cardia, must be removed. Those who swallow air must be cautioned against the bad effects of the habit. With strong dilation of the stomach through air and gases, in consequence of fermentation and stagnation of the contents, the air and gases should be removed as quickly as possible by the introduction of a rather thick, rigid tube, and a more copious formation of gases must be prevented by methodical lavage of the stomach, often with the addition of antiseptics. The diet must, for some time, consist of milk, and later of various meats taken in a minced form. Other nervous disorders must receive suitable treatment. One of the best methods of treatment for cramp of the cardia is the introduction of firm, thick tubes, which are permitted to remain in position for thirty minutes at a time. Sometimes the cramp ceases entirely after sounding one or more times. If the spasm is the consequence of the hyperesthesia of the mucous membrane of the esophagus and cardia, the sensibility is blunted by frequent soundings. In very stubborn cases of hyperesthesia with cardiospasm it is ad- visable to apply a solution of cocain hydrochlorate to the mucous membrane just before the meal, in order to prevent the appearance of the cramp. For this purpose one had best use a small sponge, satu- rated with a three per cent, solution of cocain, and fastened to the lower end of an open, rather thick, firm tube, with rounded edges, by means of a strong silk thread brought through the tube to its upper end. After introducing the tube into the cardia, the cocain solution is forced out of the sponge by pulling the silk thread, or by blow- 746 PYLORIC SPASM. ing air into the tube, and the mucous membrane may thus be anes- thetized. Another way of accomplishing this is with the Einhorn intragastric spray, by which the lower part of the esophagus and the cardia may be sprayed with cocain and menthol. With chronic cardiospasm also the methodical introduction of firm tubes is the most successful remedy. The effect may be aided by external or internal galvanization (the anode in the tube). According to an in- teresting observation of Boas, solid foods are sometimes introduced more easily than liquid ones. Before meals the foods lying in front of the cardia are to be removed as completely as possible, especi- ally when a diverticulum should have developed (rare). In both acute and chronic cardiospasm we have obtained the most permanent relief by the galvanic current. The length of the esopha- gus is determined by methods devised by Penzoldt (/. c.) and Isert Perl, and a rather large spiral electrode (Stockton’s) is introduced to a distance compelling it to be in or near the cardia; the cathode is placed on the cervical region, the anode in the cardia, and a cur- rent of twenty-five milliamperes is turned on for ten minutes. Then the same procedure is repeated with the anode on the epigastrium and cathode in the cardia. PYLORIC SPASM (Pylorospasm, Cramp, Convulsion, Spasm of the Pylorus). Cramp of the ring musculature of the pylorus is brought on by entirely different causes : it may appear with hyperesthesia, with very strong chemical irritation of the mucous membrane of the pylorus by means of hydrochloric acid (hyperacidity, super- secretion), by excess of organic acids, as well as with dilation of the stomach by gases (as a reflex neurosis), and finally also after the caustic action of toxic substances, and further as a secondary disease accompanying ulcer and ulcerating carcinoma of the pylorus. While the existence of a secondary cramp of the pylorus is generally recognized, strange to say the existence of a primary cramp of the pylorus, caused by an independent motor neurosis, restricted to the pylorus alone, is still generally denied. If one grants, however, that the insufficiency of the pylorus may appear also as a genuine motor neurosis, due to a decrease of the irrita- bility of the motor nerve apparatus of the pylorus, there is no reason to deny entirely the occurrence of a primary cramp of the pylorus, which is due to an abnormally increased irritability of the motor nerves, even though this be rare. Indeed, Stiller, one of RESULTS OF PYLOKOSPASM. 747 the most competent judges of neuroses of the stomach, assumes a primary cramp of the pylorus for the explanation of peristaltic unrest of the stomach. It is true its detection, as well as that of the secondary spasm, is very difficult, since the most important result of the same — namely, an increased peristalsis of the stomach — can not be proved with normal location and size of the stomach except by Hemmeter’s or Einhorn’s method.* The existence of a primary cramp of the pylorus becomes proba- ble if, after the exclusion of the before-mentioned causes (secondary cramp of the pylorus), as well as of organic disease of the stomach, the reaction for iodin in the saliva occurs much later than under ordinary circumstances, after the introduction of o.i iodoform into the stomach with the test-breakfast. According to A. Lockhart Gillespie (Brit. Med. Assoc., July, 1898), salol was absorbed from the stomach in a dog in whom he produced a fistula in the duodenum near the pylorus. He still found the salicyluric reac- tion in the urine, although no salol reached the small intestine. Stein (“ Wien. Med. Wochenschr.,” 43, 1892) found that salol was absorbed from the stomach, and, although not decomposed in that organ, it may appear as salicyluric acid in the urine. For these reasons the salol test can not be relied upon as informing us con- cerning the presence or absence of pyloric stenosis. The diagnosis becomes probable also when atony of the stomach appears without any assignable cause. The results of a primary cramp of the pylorus are the same, naturally, as those of the secondary. Since contents of the stomach can not pass into the intestine during the entire duration of the spasm, there must result a stagnation of the ingesta and a protracted burdening of the stomach, causing atony of mus- culature, which also becomes gradually exhausted through the energetic exertions for overcoming the increased resistance at the pyloric orifice. If the neurosis is very stubborn, the atony may pass over into a pronounced dilation, particularly if the stagnating ingesta decompose rapidly and the atonic stomach is abnormally distended with gases. *In a singular case of periodic pylorospasm occurring in a hysterical female regularly at the menstrual period, we obtained a record with our triple intragastric bag which may be characteristic of these cases. This bag (•* N. Y. Med. Jour.,” June 22, 1896) records the pyloric, fundic, and cardiac peristalsis separately on three tambours on the kymograph (see p. 80), and in this case the pyloric pen showed great spastic contractions, and tenes- mus lasting from three to five minutes before they relaxed. The pens recording the fundic and cardiac contractions were quiet during this period except for slight passive movements due to respiration and impulse of aorta. 748 PERISTALTIC UNREST. Therapeutics. — If a primary cramp of the pylorus is suspected, a digestible, non-irritating diet is to be prescribed (see chapter on Diet); every immoderate burdening and dilation of the stomach through very abundant meals, which might heighten the irritability of the motor nerves, is to be avoided. With this the bromids, pre- ferably the bromid of strontium, in liberal doses (3.0 (45 grs.) to 5.0 (75 g rs 0 P er diem), extractum belladonnae (0.02 (J- of a gr.) to 0.03 ( y 2 of a gr.)), and codein phosphate (0.02 (^- of a gr.) to 0.03 of a gr.)), chloral hydrate (10 grs. t. i. d.) are to be prescribed. Elec- tricity is a valuable adjuvant to the treatment, and should be used in the same manner as indicated for cardiospasm. Spraying the pylorus with cocain and menthol is a satisfactory treatment. Under narcosis the pylorospasm relaxes. The pylorus may be intubated by the author’s method : A large tube once passed through the pylorus will, if allowed to rest there for ten minutes, in some cases act in a very gratifying manner, allaying the spasm without any other treatment. This method constitutes a means of recognizing pylorospasm. GASTROSPASM (Convulsions of the Stomach). Gastrospasm is a neurosis in which the musculature of the stomach is so strongly contracted that the whole organ may be- come hardened like a board, and may be recognized by palpation as a resistant mass through the lax abdominal integuments. It is a very rare disease. Whether it ever occurs as an independent genu- ine neurosis of the motor apparatus, or whether, as is generally supposed, it occurs only as a secondary nervous affection, with hyperesthesia of the sensory nerves of the stomach, or as a conse- quence of a cramp of the pylorus, combined with hypertrophy of the musculature of the stomach, is still an open question. In the very rare cases observed thus far the single paroxysms of gastrospasm invariably lasted but a short time, and the quick intermission might be sufficiently explained by the enormous over- exertion of the musculature during the attack. The treatment is the same as for hyperperistalsis (Kussmaul). GASTRIC HYPERPERISTALSIS (Peristaltic Unrest (Kussmaul)— Tormina Ventriculi Nervosa). General Considerations. — Peristaltic unrest is the name given by Kussmaul to a state of the stomach first described by him, which ETIOLOGY OF H YPERPEKISTALSIS. 749 is characterized by the appearance of extraordinarily rapid con- tractions of the stomach, following close upon one another, which appear especially after meals, continuing also during the day and sometimes through the night with an entirely empty stomach. This excess of peristalsis brings about very disagreeable sensations of heaving to and fro, of unrest, and contractions in the region of the stomach which, without being really painful, — as, for example, the so-called cramps of the stomach with cardialgia, — may nevertheless annoy the patient very much. When there is an ectasia or a dis- location of the stomach present simultaneously, as was the case in all the observations up to date, these abnormally strong contrac- tions of the stomach can be seen and felt externally through the lax abdominal integument as distinct undulatory motions. The peris- taltic waves generally run from the fundus to the pylorus : that is, from left to right. Besides the peristaltic motions, in a small pro- portion of cases antiperistaltic motions were observed also ; sometimes the latter were observed to exist alone, but this is rare (Schiitz, Cohn, Glax). If the size and location of the stomach are normal, the objective symptoms are lacking entirely, and only the subjective complaints, particularly the feeling of unrest, are evident. Sometimes, also, peristaltic unrest of the small intestine coexists with that of the stomach. Increased irritability of the motor nerves of the stomach is looked upon as the cause of peristaltic unrest. Etiology. — An abnormally increased activity of the stomach may be brought about by different causes : 1. As a reflex process, through hyperesthesia of the sensory nerves of the stomach. 2. By a very strong stimulation of the mucous membrane of the stomach by HC1 (hyperacidity, supersecretion), by organic acids, the result of an abnormal fermentation of the contents of the stomach, by gases which distend the stomach to a considerable degree. 3. With an advanced stenosis of the pylorus and of the duo- denum, and, finally, it may be due to an increased irritability of the motor nerves, and may thus be the result of an independent functional neurosis. The question arises, Which of the motor nerves of the stomach take part in the merely functional illness in the case of peristaltic unrest ? While Stiller, who has paid much attention to neuroses of the 750 HYPERPERISTALSIS. stomach, traces back peristaltic unrest to a cramp of the ring musculature of the pylorus, other authors explain it by an in- creased irritability of those motor nerves which innervate the musculature of that region of the stomach lying between the cardia and the pylorus. In severe cases the anomaly of function is probably extended over all the motor nerves of the stomach, since with cramp of the pylorus alone the peristaltic motions are not so intense as with peristaltic unrest. Fleischer had opportunity of convincing him- self of this in a case of dilation of the stomach in which the greatly contracted pylorus could each time be felt distinctly through the lax abdominal integuments. With normal size and location of the stomach the peristaltic motions are not visible in the epigastrium, in spite of the pres- ence of peristaltic unrest, on account of the thickness of the abdominal integument and because a part of the stomach is under the liver; it is thus very probable that many cases escape detection. Sexual excesses, repeated intense emotions, an unsuitable mode of living, general nervousness, as well as anemia, increase the dispo- sition to this disease. Symptomatology. — If a stomach which is dilated or dislocated downward is seized with peristaltic unrest, the symptoms are, in decided cases, so characteristic that they can not easily be over- looked or mistaken. The very strong contractions of the gastric musculature, repeating quickly, can be distinctly seen and felt as un- dulatory motions, especially when abdominal integument is relaxed. If the stomach, at the same time, contains liquids and gases, the peris- taltic waves are often accompanied by strong, gurgling noises which can be heard at some distance. These undulatory motions, caused by restless action of the muscles, generally run in the direction from fundus to pylorus: that is, from the left above to the right below, more rarely also in the reverse direction of right to left. In some cases only antiperistaltic waves have been observed. By the con- traction of the muscles, the fundus of the stomach may at times be distended to the size of a child’s head, so that it strongly arches up the abdominal walls. After a time the elevation sinks, to appear in another region of the stomach. At the height of the contraction of the muscles there may be a slight circular constriction or furrow seen in the middle of the stomach, dividing the organ into two nearly equal parts, so that it temporarily assumes the shape of an hour-glass. SY M PTO M ATO LOGY. 75 * Since the muscular undulations can be observed only with a dilated or dislocated stomach, they naturally extend beyond its normal location ; if peristaltic unrest of the small intestine exists simultaneously, the undulations extend also over a part of the hy- pogastric region, and even with an empty stomach a rolling and rumbling noise, originating in the intestines, can be heard. Slight degrees of peristaltic unrest occurring when the stomach is in a normal position are recognizable by the aid of the X-rays and fluoroscope. The patient’s stomach must contain about one liter of milk mixed with one teaspoonful of subnitrate of bis- muth. While energetic contractions of the stomach hasten the execu- tion of its normal functions, an excessive peristalsis has a directly injurious effect, and causes manifold disturbances of digestion. Patients frequently complain of a lack of appetite, belching, nausea, and vomiting. If the peristaltic unrest is very stubborn, the patients may suffer a loss in nutrition, so that the suspicion seems justified that malignant neoplasm is developing. If the peristaltic unrest continues also through the night, the state of mind is generally much depressed, because patients are constantly re- minded of their stomach and their disease ; any neurasthenia which may be present is often considerably increased. If the small intestine is also the seat of active peristaltic unrest, intestinal gases and liquid contents sometimes regurgitate into the stomach. The eructations are then very foul-smelling, and often feculent masses are vomited, which may, exceptionally, even contain scybala. The demonstration of scybala in vomited matter indicates that the peristalsis of the colon, which generally is not concerned in peristaltic unrest, is considerably increased. In spite of peristaltic unrest of the small intestine, very stubborn constipation and meteorism often occur, because the colon is, as a rule, pacific during these enteric contortions. With normal size and location of the stomach the objective signs of peristaltic unrest are wanting, and sometimes the disagreeable sensations of unrest in the region of the stomach constitute the only subjective symptom of the disease. Prognosis. — If the peristaltic unrest is the result of a genuine, independent, or symptomatic neurosis, the prognosis on the whole is favorable. When injurious substances before mentioned are kept away, and the primary diseases — neurasthenia, anemia — can be 752 HYPERPERISTALSIS. removed, the peristaltic unrest, as a rule, soon recedes with suitable mode of living, diet, and with methodical use of electricity. Diagnosis. — In order to diagnose with certainty that type of peristaltic unrest which is an independent, genuine motor neurosis, it is necessary first to exclude those other diseases which also cause an increased peristalsis of the stomach. The so-called cramps of the stomach with cardialgia are accompanied with more or less severe boring, gnawing, or cramp-like pains, and, therefore, are generally easily recognized. Whether the increased peristalsis is the result of a very strong irritation of the mucous membrane of the stomach by hydrochloric acid, organic acids, or by gases which distend the organ to excess, may generally be easily determined by a repeated chemical analysis of the stomach contents ; further, the gastralgia sometimes ceases entirely when the stomach has been emptied by the tube and is thoroughly cleansed (which is not the case with peristaltic unrest). The increased peristalsis of dila- tion resulting from stenosis of the pylorus or duodenum is also arrested by lavage. The diagnosis is very difficult with normal size and location of the stomach. In these cases the author’s method of graphically recording the motor functions by the deglut- able stomach-shaped bag is, perhaps, the only reliable means of settling the differential diagnosis between peristaltic unrest of the stomach and that of the intestines. In fact, in all neuroses of motility the intragastric stomach-shaped bag gives most valuable informa- tion of the nature and intensity of the peristalsis. (See p. 80.) One may suspect peristaltic unrest when the symptoms recede rapidly after methodical application of electricity, arid when other nervous disturbances occur coincidently. In the distinction of peristaltic unrest of the stomach from that of the intestine one should ascertain whether the rolling and rumbling is still audible with an empty stomach, and whether the peristaltic motions can also be perceived outside of the limits of the stomach. If, with an empty stomach, every splashing noise is constantly absent, and if the sounds appear again shortly after drinking water, this argues for peristaltic unrest of the stomach. If dilation or dislocation of the stomach can be excluded, the visible peristaltic motions are to be ascribed to the intestines. Leube has described cases in which loops of small intestine were evidently pushed up between the stomach and the abdominal wall while in active peristalsis. Sedatives, like the bromids, opium, and belladonna, are said to TREATMENT OF H YPEKPEK ISTA LSIS. 753 exert a more controlling effect on the intestinal than on gastric hyperperistalsis. Therapeutics. — The sufferer must be urged to keep away from injurious influences, such as sexual excesses, mental shocks, and overexertions, etc., and lead a quiet, regular mode of life. If the peristaltic unrest is a partial or resultant effect of a decided neuras- thenia or anemia, a protracted sojourn in the country, in the mountains, at the seashore, and hydropathic procedures (cold rub- bings, baths) will influence favorably the nervous system and the composition of the blood ; the anemia must also be fought by a strengthening, easily digestible diet (scraped meats), and by iron and arsenic preparations. In severe cases in which the peristaltic unrest continues through the night, resting in bed and a mild diet (milk, soups) are recom- mended, and cold bandages or packings of the stomach should be tried, and if these do not relieve, then warm cataplasms. Every immoderate loading of the gastric walls, as well as every severe dilation of the stomach by means of gases, is to be strictly avoided, in order not to increase the irritability of the motor nerves. Kussmaul obtained very favorable results by the internal and external applications of electricity. In the former case the anode, by means of the tube, is inserted into the stomach, partially filled with a small quantity of a normal salt solution (0.6 per cent.), and then slow rubbing motions are to be made with the cathode externally in the region of the stomach ; in external galvanization the anode is used for the last-mentioned movements, while the cathode is placed on the sternum. I have had satisfactory results with exclusive rectal feeding in two cases of peristaltic unrest in which the stomach was in the normal position. The rectal nutri- tive enemata were continued for sixteen days; thereafter the symp- toms disappeared. Of the medicines, sodium, ammonium, or strontium bromid, — in doses of three to five gm. (45 to 75 grs.) in twelve hours, — extract of belladonna, dose, 0.008 to 0.013 (% °f a g r - to of a gr.), or codein phosphate, dose, 0.02 to 0.03 gm. of a gr. to y 2 of a gr.), are to be recommended. The bromid of strontium, 20 grs. four times daily, has my preference. Exclu- sive feeding by the rectum for one week is more effective when combined with rest in bed and the use of the bromids. In a per- sistent case of peristaltic unrest in a gouty patient I obtained 754 NEUROSES OF THE STOMACH. very good results from salicylate of sodium i scruple, with bismuth subnitrate 16 grs., three times daily. NERVOUS ERUCTATION. This is a frequent symptom in hysteria, neurasthenia, and allied neuropathic conditions. It is said to be particularly frequent in the sexual neuroses. The belching up of tasteless or offensive gases is a frequent symptom in most gastric diseases. In fact, it occurs at times in every normal person, and then consists of the sporadic expulsion of air that has been swallowed with the food, or of C 0 2 that has been taken in with beverages, or has been formed by fermentation of the food. The pathological condition which occurs in neurasthenia consists of the explosive evacuation of tasteless gas in large quantities. The attacks are usually parox- ysmal, and the gas that is expelled is generally air, which is not formed in the stomach, but which has been swallowed. Every time air is eructated from the stomach the closure of the cardia must be opened, and with a frequent repetition of this a permanent relaxa- tion of the cardia may develop. The muscular development of the pylorus being much stronger, this orifice is not so easily opened by gas. We have known nervous individuals, particularly hysterical patients, to belch up air during the entire day, and often during the night. Air can be aspirated into the stomach when the cardia is relaxed and the esophagus is closed, either in consequence of a negative thoracic pressure when the vocal cords are closed, or be- cause the lumen of the stomach expands and dilates under nervous influence. On the other hand, some nervous patients have the bad habit of intentionally or unconsciously swallowing air until the stomach is expanded, when the same air is eructated with explo- sive violence. In one of the patients of Cartellieri (“ Wiener allge- meine med. Zeitung,” 1885, S. 3), 2500 eructations occurred in one hour. Some patients have dyspeptic symptoms, while in others digestion is not disturbed. I have personally known a neuras- thenic colleague who could eructate whenever called upon to do so. It is probable that in this case the air that is swallowed does not reach his stomach, but gets no further than the upper part of the esophagus, when it is again expelled. Oser has explained the aspiration of air into the stomach, assuming that it acts on the principle of an elastic balloon — the contraction of the longitudinal muscle enlarging the gastric lumen and thereby sucking in air, NERVOUS ERUCTATION. 755 and the circular muscle contracting it again and thereby expelling it. This would not explain all cases, because in some hysterical patients the eructation is so rapid and uninterrupted that there seems to be no time left for swallowing air in this manner. It is probable that a clonic spasm of the pharyngeal muscles may exist here, persistently pressing air into the esophagus, which eventually reaches the stomach, but generally is expelled from the esophagus. (Bouveret, /. c., “ Aerophagia.”) Esophageal eructation and vom- iting may be produced by hysterical patients at will. Cartellieri asserted that his patient (/. c .) had no time to swallow air during the attack, and Ewald raises the question whether these attacks are really nervous eructations, or only simulate them. Pneumatosis. — This is a condition of the foregoing disease, in which the stomach is abnormally expanded with air, producing a sensation of unpleasant distention and dyspnea. When the air escapes into the mouth or intestines, the torturing feelings cease. The suffering may be permanent or only periodical, and has been attributed to a spasmodic closure of the cardia and pylorus. The dyspnea that occurs in these cases has much similarity to the “ asthma dyspepticum ” of Henoch. Pneumatosis may be easily recognized by an inspection and percussion of the inflated stomach, which, of course, should be differentiated from a possible distended transverse colon. In many cases persistent constipation will be found to be an etiological factor, for in these cases the pneumatosis rapidly improves when the bowels become regular. A possible gastric dilation and atony must be excluded. Treatment. — The patient and his attendants must be instructed that the eructation and the pneumatosis are largely a habit, and that by close observation of the patient he or she can be inter- rupted in the act of swallowing air. Penzoldt cured a patient of this kind who had been uninterruptedly swallowing and eructating air, by making him keep his mouth open for a half-hour, as it is impossible to swallow air when the mouth is open. The eructation ceased entirely, and the patient became convinced that the swallow- ing of air was the cause of his suffering. The explosive eructa- tions of hysterical patients are best treated by methods directed toward the psychical condition of the case. Quincke has seen cures by introducing a thick, soft stomach-tube, and permitting it to rest for a while in the esophagus. The cases that depend upon aspira- tion by alternate expansion and contraction of the stomach are, in my experience, benefited by the intragastric application of the gal- 756 NEUROSES OF THE STOMACH. vanic current. The neurasthenic foundation of the disease should receive careful attention — thus nervous eructation and pneumatosis have, in my experience, been repeatedly cured by a course of surf- bathing, as well as the Scotch douche applied to the epigastrium. Cold sponging and massage are very useful aids in treatment. Among the drugs that have been recommended are small and frequently repeated doses of arsenic, belladonna, or atropin, hypo- dermic injections of morphin, and cocain. Boas obtained good results from the following pill : R. Extract, physostigmatis, o. 13 gr. ij Extract, belladonnse (Ale.), 0.25 gr. iv Strychnin sulphate, 0.03 gr. ss. M. Fiant pill, No. xx. SiG.— One pill three times a day. Spraying the pharynx with solutions of cocain and menthol, and the internal administration of bromid strontium are available thera- peutic measures. Neurasthenia depending on uric acid diathesis frequently causes nervous eructations, for which salicylate of sodium is of more value than the bromids. NERVOUS, HABITUAL, OR REFLEX VOMITING. In the classical experiments of Magendie the stomach of an animal was replaced by a pig’s bladder, and after tartar emetic was injected into the blood, the contents of the bladder were vomited ; this experimenter, accordingly, concluded that the stomach had nothing to do with the act of emesis, but that it was brought about by action of the abdominal muscles. Tintani, however, showed later on that the experiment of Magendie no longer succeeds when the cardia still remains intact and is not cut away ; therefore the cardia, inasmuch as it can prevent vomiting, must be concerned in the act of emesis, which was found to consist of firm closure of the pylorus, opening of the cardia, while powerful peristaltic and anti- peristaltic waves traveled over the stomach. The main force for emesis is then furnished by the abdominal muscles, which are ener- getically assisted by the contractions of the stomach itself. There are three forms of nervous vomiting : (1) The cerebral or spinal vomiting (also known as central vomiting), which is caused by di- rect or indirect stimulation of the vomiting center in the medulla oblongata from other irritated foci in the brain and spinal mar- row. (2) Nervous vomiting, occurring as a symptom of hysteria or neurasthenia. (3) The reflex vomiting, in a more restricted NERVOUS VOMITING. 757 sense, brought about by reflex irritations from various other organs in the body. Cerebral vomiting is a frequent symptom in organic diseases of the brain and its membranes, particularly when they are asso- ciated with circulatory disturbances or changes in intracranial pressure occurring more or less suddenly. It has been observed in acute inflammatory processes, like encephalitis and meningitis, also with cerebral abscesses, tumors, and focal diseases. It may result from acute anemia or hyperemia, and after concussion of the brain. It is said to occur also with vivid emotional affections, and after intoxication by opium, chloroform, ether, nicotin, and also in uremia. Spinal vomiting in diseases of the cord is rarer, but it is quite frequent in exophthalmic goiter and in tabes dorsalis, in which it occurs in form of the gastric crises, first described by Charcot. Gastric Crises. — In a majority of cases the gastric crises are accompanied not only with severe vomiting, but with gastric hyperesthesia and hyperchylia. According to Leyden, the vomit- ing may be absent entirely. The attack begins without any pro- dromal symptoms. In the midst of well-being the patients complain of intense, spasm-like pains in the stomach, particularly in the epi- gastrium, which radiate to the sides and to the back. The face is pale, the pulse is small, soft, and rapid, there are vertigo and palpitation of the heart. The bowels are constipated, the ap- petite is lost, and thirst is great. At the same time there are great prostration and weakness and a clinical picture of severe collapse. Although the patients drink large quantities of water, they pass very little urine, partly because the water is again vomited, or because it can not enter the intestines on account of an existing pyloric spasm. The abdomen is much retracted on account of clonic contractions of the stomach and intestines, as well as of the abdominal wall. Very soon, copious vomiting begins. First food, then bile, mucus, and particles of blood are vomited. The reaction of the vomit, as a rule, shows hyperacidity. Von Noorden (“ Charite Annalen,” 1890, S. 166) and Seymour Basch have re- ported attacks of gastric crises in which the acidity for free HC 1 was normal or subnormal. The degree of acidity will natur- ally vary with the length of time that the vomited ingesta have remained in the stomach. After abundant vomiting transient relief is generally experienced, and in mild attacks this may be the end of the crisis ; but in severe attacks the vomiting may occur 50 758 NEUROSES OF THE STOMACH. hourly, continuing to the evening, with very short intermissions. During the night the attacks generally cease, to return again on the following day. This course of symptoms may repeat itself in eight to ten days, by which time the debility of the patient is very great. The suffering may cease just as rapidly and suddenly as it came. The vomiting stops, the appetite improves, and the general condi- tion of the patient slowly convalesces. If gastric crisis occurs in a case of advanced tabes, its recognition is not difficult, but when it occurs as one of the very first symptoms of tabes, the correct diag- nosis may be difficult. In that case we must test the patellar re- flexes, the reflexes of the pupil, Romberg’s symptom (increased incoordination of movements by placing feet together and closing eyes), and inquire concerning the existence of lancinating pains. In case the connection with tabes is not established, gastric crises may be mistaken for gastroxynsis, hemicrania, or hyperacidity. Hemi- crania — intense, one-sided headache — is rarely complained of in gastric crises. The gastric pains in hemicrania are insignificant. Gastroxynsis occurs only in men, after severe mental exertion or after well-known toxic influences, and is always incited by certain opportune and traceable causes, which is not the case with gastric crisis. Periodical Vomiting (Leyden). — This is a combination of symptoms in which the prominent feature is vomiting that returns in regular intervals. In some cases the days of the paroxysm of the attack may be predicted with tolerable accuracy. The attacks begin without any marked prodromal symptoms, in the midst of apparently good health. Gastralgia may introduce the attack or may follow it. The appetite is lost, pulse small and frequent, tongue coated and dry. The patients may have intense headache and even slight delirium. The clinical picture is very similar to that of the gastric crisis. The character and the reaction of the vomit are essentially the same. The duration of the attack varies between twenty-four hours and fourteen days ; some patients have lancinating pains in the extremities in place of gastralgia. Toward the end of the attack the vomiting gradually ceases, and the remain- ing complaints slowly disappear. The characteristic of periodical vomiting is that the attacks occur at certain definite intervals of from two to ten weeks. The repetition occurs with great regularity, and the disease may last many years. The prognosis is therefore a very doubtful one. The distinction from gastric crisis is made by the typical periodicity, and the pres- NERVOUS VOMITING. 759 ence of great hyperacidity of the vomit in the crisis. Periodical vomiting appears occasionally as a primary, idiopathic neurosis of the vagi. It has been known to occur with hydronephrosis, with floating kidney, diseases of the uterus and ovaries, with intestinal entozoa, and nicotin poisoning. Nervous Vomiting in the Course of Neurasthenia and Hys- teria. — This vomiting is found more frequently in hysteria than in neurasthenia. If it occurs in neurasthenia.it is associated with marked sensitiveness of the lower thoracic and the upper lumbar vertebrae to the electrical current (M. Rosenthal). The patients frequently complain of severe pain in the gastric region, pointing to a hyperesthesia of the sensory nerves, which may probably be the cause of this kind of vomiting. Stiller gives the fol- lowing points which are characteristic of vomiting of nervous origin: (i) The facility of the emesis. (2) The independence of the quality and quantity of the ingesta. (3) The capricious- ness with which very bizarre articles of diet are frequently retained to the exclusion of others. (4) Sometimes the elec- tive vomiting of certain substances which seemingly are sepa- rated from the mixed chyme. (5) The carelessness with which the patient endures the habitual sickness. (6) The tolerance of the body to the effect of inanition caused by the habitual vomiting, even when the metabolism is much reduced. (7) The extraordin- ary influence of the slightest external and internal causes that act on mood or temperament. (8) The frequent occurrence of emesis when no food has been taken and the stomach is apparently empty. {9) The presence of other nervous symptoms alternating or con- temporaneous with the vomiting. To these Boas adds (10) the absence of important secretory or motor disturbances. In some of these cases the vomiting occurs almost every day, occasionally after each meal. In other cases the attacks occur at longer or shorter intervals, either spontaneously or after severe influences exerted upon the psychical sphere. Cases have been repeatedly observed in which only the liquids have been expelled, and in others only the solids. Sometimes the vegetable and carbohydrate foods are vomited and proteid food retained, or vice versa. Nausea and retching are absent in the vomiting of hysterics, which occurs with- out any exertion. Juvenile vomiting rarely occurs by itself, but is rather an expres- sion of a dyspepsia developed in school-children as a result of mental overexertion. The symptoms are the following : dyspeptic 760 NEUROSES OF THE STOMACH. complaints, gastralgia, vomiting, great pallor, dilation of pupils, slowing of the pulse, constipation. In all of these cases improve- ment follows when the children are removed from school and allowed to rusticate in the fresh country air (Leyden, “ Ueber period. Erbrechen,” etc., “ Zeitschr. f. klin. Med.,” 1882, Bd. iv, S. 605). Reflex Vomiting in a More Restricted Sense. — Strictly speaking, vomiting is almost always a reflex act, and the separation of other forms of vomiting from reflex vomiting is justifiable only on didactic grounds. There is hardly an organ which could not produce this form of vomiting when it is in a state of irritation. The peripheral irritations which cause this reflex vomit- ing are, among the first, those which strike the sensory and motor nerve-endings in the esophagus, the posterior pharyngeal wall, the epiglottis, the soft palate, and the root of the tongue. All organs that are supplied by branches of the vagus — so particularly the abdominal organs — may, under pathological conditions, excite an attack of re- flex vomiting. It may occur as a result of constipation, meteorism, lead colic, irritation by foreign bodies, and intestinal parasites. It is one of the first symptoms of strangulated hernia, and of conditions of irritation in the peritoneum. Abscess of the liver, perityphlitis, renal and hepatic colic are associated with reflex vomiting. It has been known to occur by the invasion of the ascaris lumbricoides into the ductus choledochus, emboli in the kidney, liver, pancreas, and spleen, floating kidney, and severe concussion or contusion of any abdominal organ. Diseases of the female sexual organs are a prolific source of this form of emesis. It is not the severe ana- tomical diseases of these organs that most often cause these attacks, but preferably the slight, inconsiderable affections. Normal men- struation and pregnancy are occasionally accompanied by emesis. The so-called pernicious vomiting of pregnancy may be caused by a variety of conditions, although its pathogenesis is still obscure. When vomiting is uncontrollable in a female in whom the evidences of pregnancy are unmistakable, the embryo should be removed and the uterus curetted before prostration becomes too great. Fleischer states that this should be done in order to save the life of the mother and eventually that of the child (/. c ., p. 977) ; the pernicious vomiting of pregnancy occurs, however, at such an early period in our experience that the child would not be viable. Every form of severe vomiting, when it continues for a week or more, will eventually produce hematemesis from local ischemias PROGNOSIS AND DIAGNOSIS OF NERVOUS VOMITING. 761 produced by the convulsive gastric contractions during the emesis. In a patient that died at the Maryland General Hospital in April, 1897, the young woman, who was undoubtedly pregnant, and who refused to be curetted, vomited and purged blood in the second week so that the practitioner who presented her for admission stated that she had undoubtedly a gastric ulcer. At the autopsy, which occurred three weeks after the beginning of the attack, an embryo between two and three months old was found within the uterus, while nowhere in the stomach could a lesion be found ex- cepting large ecchymoses, some of them attaining the size of a five-cent piece, and scattered over the entire surface of the stomach, which, in our opinion, had been caused by the intensely spastic contractions of the stomach, producing ischemia. Displacements of the uterus, pelvic exudates, parametritis, inflammations and ulcerations of the uterine mucosa, myomata, and ovarian diseases may cause reflex vomiting, which is much rarer with the diseases of the male sexual organs. Nevertheless, it is occasionally ob- served with injury or inflammations of the testicles and in epididy- mitis. Chronic inflammation about the nasal mucous membrane, polypi, and hyperplasia of the upper air-passages have been re- corded as producing the disease. Eichhorst has repeatedly ob- served reflex vomiting in certain individuals on hearing very shrill tones. Von Troeltzsch has called attention to the fact that irrita- tion of the external auditory canal may cause emesis. Prognosis of Nervous Vomiting. — The prognosis will vary with the fundamental causative disease. Gastric crises, when they occur in advanced tabes, may cease entirely after a time, although the fundamental disease continues and even becomes worse. Peri- odical vomiting, which occurs after insignificant disturbances in other organs, which get well without difficulty, may stubbornly persist after the fundamental disease has been cured. The prog- nosis is favorable whenever the causes can be recognized and completely removed.* * A case of severe nervous vomiting which had persisted for two years under my observation defied all treatment : electricity, lavage, Weir-Mitchell rest-cure, sedatives. All foods were vomited. For two months a membranous colitis prevented rectal feeding, and the life of the patient was maintained by hypodermic injections of sterile olive oil. Periodical pyloric spasm existed at the same time. Professor Howard A. Kelly, after an exploratory incision, found nothing abnormal with the stomach or intestines, no adhesions, pelvic organs, liver, and spleen normal. But the pylorus seemed somewhat smaller than it should be, and a pyloroplastic operation was done (January 19, 1900). It is too early to judge of the effects of this operation, but one week thereafter the vomiting had not re- 762 NEUROSES OF THE STOMACH. Diagnosis. — The majority of the forms of nervous vomiting can be determined after an exhausting examination of the entire body, the urine, the blood, and gastric contents. A careful study of the previous history is indispensable. Nervous vomiting, as has been said, may be in rare cases an idiopathic vagus neurosis (Leyden), but in most cases some palpable cause for the vomiting can be detected. Prominent among these are dislocated kidneys, hydro- nephrosis, uterine and ovarian diseases, entozoa, and nicotin poisoning. A careful examination of the fundus of the eyes, of the ears, and of the nose, mouth, pharynx, and larynx should never be omitted. Treatment. — Whenever possible, the treatment must be di- rected to the underlying causal disease. When the various morbid states of other organs, which have been mentioned in the etiology and symptomatology, can be excluded after application of all methods of diagnostic technic, only then is a purely symptomatic treatment justifiable. Hysteria and neurasthenia are to be met by hydropathic procedures, or by absolute rest, abstention from mental and emotional excitement, and a sojourn in the mountains or at the seashore. In most cases the greatest possible rest, and strict avoidance of psychical disturbances will be indispensable. Gastral- gic pains and hyperesthesia can be relieved by a hot cataplasm on the stomach, but the application of the galvanic current anode on the stomach or in the stomach, and cathode alternately on the sternum or spinal column will be more efficacious. The internal gastric douching with warm water, and, as we have found, spraying of the inside of the stomach with solutions of menthol and cocain, are also generally followed by cessation of the pain. In vomiting of pregnancy rectal feeding and six grains of the basic orexin in a gelatin capsule three or four times a day should be tried first, but cureting of the uterus should not be delayed too long. The fol- lowing formula we have found efficacious in the treatment of this form of vomiting of the non-pernicious type : R- Cerii oxalatis, .... gr. lx Cocain hydrochlor. , . . 0. 2 gr. iij Menthol, gr. xij Bismuth salicylatis, . . 4.0 Elixir simpl., . . . . q. s. 180.0 f^vj. SlG.- — One-half fluidounce on an empty stomach four times daily. turned. The case is mentioned only to show that very severe cases of nervous vomiting may exist without observable anatomical lesions ; may endanger life by progressive emaci- ation. TREATMENT OF NERVOUS VOMITING. 763 Hypodermic injection of -J- of a grain of morphin, together with of a grain of atropin sulphid, proved helpful in a number of cases. The idiosyncrasy of the patient concerning diets should be care- fully studied. A priori, “ no diet can be suggested that shall be universally applicable to all cases.” The ingestion of liquids must, as a rule, be very much limited, and thirst relieved by colon enemata. If every meal is vomited, it is best not to permit the ingestion of larger quantities of food, but simply to give nourishment in very small quantities — iced milk, champagne, cold tea or coffee, or egg- albumen with brandy, or clam bouillon in tablespoonful doses. Superacidity must be treated according to principles laid down in the chapter on this subject. When there is abnormal hyperesthesia of the stomach, it is well to feed the patient by rectal enemata for about a week to ten days, according to methods described in the chapter on Dietetics. The most effective sedative that we have is morphin, particularly the hypodermic injection of of a grain, together with of a grain of atropin sulphate. The following suppositories are useful when we do not wish to create an adapta- tion to morphin : R. Extract, belladonnse, 0.2 gr. iij Codein phosphatis, 0.8 gr. xij Butyr. cacao, q. s. Supposit. No. xii. Sig. — I nsert one suppository every two hours during the attack. When the nervous vomiting persists, even during the night, the bromids, together with chloral hydrate, are of approved efficacy. I am in the habit of giving thirty grains of bromid of strontium with ten grains of chloral in peppermint water, repeated every three hours until sleep supervenes. We have also found the fol- lowing combination to be a reliable means of combatting this neu- rosis : R. Menthol, 1.0 gr. xv Cocain hydrobromatis, . . . 0.4 gr. vj Aquae chlorofbrmi, f^iv Spir. vini gallic., 60.0 Sig. — One tablespoonful three times a day, largely diluted. M. In the treatment of the gastric crises Boas has found that iodid of potassium and bromid of sodium exert very favorable influ- ences in diminishing the frequency and intensity of the attacks. 7 6 4 NEUROSES OF THE STOMACH. The use of the constant current, with the anode within the stomach and the cathode over the spinal cord in the cervical region, is gen- erally followed by a very marked palliative effect. Chloroform, three to five drops given on sugar, ammoniated tincture of valerian, twenty-five drops p. r. n., and the compound spirits of ether, fifteen to twenty drops p. r. n., might be tried, but in our experience they are rarely efficacious. Basch (/. c.) made comparative therapeutic studies with cerium oxalate, strychnin, and antipyrin in the treat- ment of tabic gastric crises. The results were not encouraging with any of these. For the control of vomiting in tabic gastric crises the following is about the most effective combination I have experience with : R . Strontium bromid, Sodium bromid, aa 3.0 gr. xlv Morphin sulphat., 0.065 gr. j Essentiae pepsin. , 200.0 ^viss. M. Sic. — One tablespoonful every two hours. INSUFFICIENCY OR INCONTINENCE OF THE CARDIA. Incontinence of the cardia, due to paresis or paralysis of the motor nerves of the ring muscle, is a comparatively rare malady, though somewhat more frequent than that of the pylorus. It appears either as an independent disease, or as a partial or result- ant phenomenon of other neuroses. The relaxation of the cardia produces an effect directly opposite to that of cramp of the cardia. While the latter, as is well known, prevents the removal, by eruc- tation, of the air and gases introduced into the stomach during meals, as well as that of liquid or solid contents of the stomach, insufficiency of the cardia, on the other hand, much facilitates it. When the relaxation of the cardia is accompanied by an increased irritation of those motor nerves which innervate the dilator of the cardia, so that by the spasm of the latter the esophageal orifice of the stomach is actively enlarged, energetic peristalsis of the stomach, with the additional influence of the abdominal pressure, will raise portions of the gastric contents into the esophagus, and even into the mouth. The firmness of the cardial closure, even under normal circum- stances, seems to vary greatly in different individuals. While many persons vomit only with difficulty, — since the resistance at the esophageal orifice of the stomach is greater, so that they have to REGURGITATION. 765 make use of almost all known remedies and devices in order to overcome it, — and even then eject only a portion of the contents of the stomach, others vomit with exceeding ease, and they succeed, with only a moderate contraction of the abdominal muscles, in emptying the stomach entirely through vomiting. In one and the same individual the closure of the cardia may vary at different times. At times small quantities of ingesta come up again into the mouth after eating, while at other times, with the same food and the same fullness of the stomach, this does not occur. If only small quantities of the contents of the stomach come up into the mouth, now and then, this does not yet constitute an abnor- mal condition ; one should only consider it abnormal when large quantities of ingesta come up after eating, and when this is repeated frequently, almost regularly every day for a considerable period of time. If the masses which come up are expectorated, the whole process is called regurgitation ; but if, on the other hand, they are swallowed again, it is called rumination (merycism, remastication), even when the regurgitated foods are not chewed again, which is observed in a small number of patients. Concerning the causes of regurgitation and rumination, opinions still differ greatly at the present time. Some authors trace both conditions to a permanent relaxation of the cardia, but the presence of the deglutition sounds is an argument against a permanent incon- tinence, according to Ewald ; other authors assume a temporary insufficiency of the cardia, and still others, in addition, an increased irritation of the motor nerves — and eventually also of the sensory nerves — of the stomach. According to M. Rosenthal, regurgitation and rumination are caused by an increased irritability of the vagus, and with this also an increased irritability of the motor nerves lead- ing from it and supplying the dilator cardiae, which causes a spasm of the latter, and through this an active enlargement of the esopha- geal orifice of the stomach. Whether the disease is of central or peripheral origin is at present also impossible to decide. Regurgitation. — At a longer or shorter period after meals large quantities of the liquid and solid contents of the stomach are at first involuntarily brought up again into the mouth, and are then expectorated. With protracted duration of regurgitation the patient generally learns how to facilitate the ascension of the ingesta by means of rather severe contractions of the musculature of the abdomen. According as regurgitation takes place in the first or second period of the digestion of the stomach, the regurgit- 766 NEUROSES OF THE STOMACH. ated food particles have either the same taste as in eating, or they taste sour (HC 1 ) or bitter (peptone). Regurgitation is not easily mistaken for vomiting, since the sensations of nausea experienced before and after the latter are entirely lacking with regurgitation. Regurgitation takes place without any especial exertion on the part of the patients, and is easily distinguished from the retching forth of foods previously eaten, in cases of stenosis or the formation of diverticula in the esophagus — that is, from the rising up of the same into the mouth, when the diverticulum is full and runs over. The difficulties of deglutition, the result of sounding the esopha- gus, as well as the constant absence of hydrochloric acid in the regurgitated masses, make a sure differentiation of the two first- mentioned diseases possible. Most patients are able to suppress regurgitation, but in a few cases they do not succeed in this, how- ever much they try. If copious quantities of the contents of the stomach are regurgitated in quick succession and are expectorated, the general nutrition may suffer considerably; but generally these patients have a very hearty appearance. Other nervous disturb- ances — signs of hysteria or neurasthenia — may be present coinci- dently. With protracted duration, regurgitation may develop into rumination. The prognosis is generally favorable with regurgitation, since the state of nutrition remains good, and if disturbances of nutrition appear, the patient often can be induced to swallow the ingesta which have risen into the mouth and to energetically prevent their coming up again. Therapeutics. — Regurgitation is promoted by hasty eating and quick swallowing of insufficiently chewed foods, especially when the latter are of difficult digestion ; a diet should, therefore, be pre- scribed which is easily digestible, and the patients should be directed to eat slowly and chew thoroughly. Gladstone’s sug- gestion is to give each morsel of food one bite or grind for every tooth in the mouth — i. e., 32 — before it is swallowed. It is best for the patients to eat in the company of such persons whose good opinion they value, so that they avoid expectorating the ingesta which have risen into the mouth, and will rather swallow them again endeavoring to combat regurgitation to the utmost of their power. If indications of hysteria or neurasthenia can be shown, these diseases are first to be treated. In stubborn cases the swallow- ing of small pieces of ice is recommended (Alt), which may reflexly induce the musculature of the cardia to contract. In addition, mas- RUMINATION. 767 sage of the epigastrium, internal and external galvanization and faradization, as well as internal administration of strychnin nitrate (0.003-0.006) are indicated. The galvanic current should be applied in the same manner as in cardiospasm. RUMINATION, OR MERYCISM. Patients afflicted with this neurosis return the ingesta from the stomach through the esophagus back into the mouth sooner or later after they have been swallowed. This is not only done without nausea, but apparently with a certain enjoyment. The raised food is rechewed, and either swallowed again or expectorated. This occurs habitually several hours after meals and without the least exertion. Rumination in the human subject has been known for a long time. Fabricius Ab. Aquapendente described the disease in 1618. As the knowledge of physiology of older practitioners was very limited, and they had no conception of the functions and mechanism of gastric digestion, the most peculiar hypotheses were developed in explanation of this very interesting neurosis. It was firmly believed that ruminants descended from parents with horns, or that they at least had a horned father, or had been nursed from the udder of ruminating horned animals. It was also believed that the stomach of human ruminants was divided into several sections by partitions, as we find them in cattle. After it was found at autopsies that ruminants possessed stomachs of the same structure as all other human beings, the profession gradually accepted the neurotic explanation of the malady. Etiology. — A neuropathic constitution is a frequent factor in the development of rumination. Heredity seems to have some effect in the matter, as ruminating fathers have been known to have rum- inating children. The element of imitation and suggestion can, however, not well be eliminated under this question of heredity. Freund and Korner have described a case in which two children developed this habit in imitation of their ruminating governess. The disease seems to be more frequent in men than in women. It occurs in all classes of society and at all ages. The following are some of the causes assigned to rumination : Sexual excesses, mas- turbation, fear, terror, anger, psychical irritations, and the very hasty deglutition of badly masticated food, particularly when it exists exclusively of vegetables, injury to the epigastrium, achlorhydria, obstinate constipation, and gastro-enteritis. It is claimed by Dehio ;68 NEUROSES OF THE STOMACH. that whooping-cough may be followed by this disease ; this is very plausible, because pertussis brings on frequent vomiting, and there- by an incontinence of the cardia. Although the disease has been known to occur in persons of high intellectuality, a large number of ruminating patients belong to the class of neurasthenics, and hys- terical, hypochondriacal, epileptic, anemic, choreic, and idiotic indi- viduals. The disease has been studied by Bourneville and Seglas, Dehio, Alt, Boas, Bear, Ducasse, Decker, Einhorn, Oser, Ponsgen, Johannessen, Lebert, M. Rosenthal, and E. Singer. In the “ N. Y. Med. Record ” for June 12, 1896, Dr. H. A. Minas- sian reports an interesting case of merycism with achlorhydria and hyperperistalsis which was cured by hydrochloric acid, exclusion of fluids, and exercise of self-control. In the same journal for July 10, 1897, Andrew Halliday, M.B., a physician of Nova Scotia, who personally has the power of regurgitation and rumination at will, gives the analysis of his own stomach-contents: Forty-five to sixty minutes after a Ewald test-meal the total acidity was 45 to 55. The free HC 1 was 0.124 to 0.1604 per cent. His motility seems normal. These two cases suffice to show the variability of the state of secretion and motility in merycism. Symptomatology. — The regurgitation of ingesta from the stomach into the mouth is usually at first voluntary, but later on involuntary. The rumination differs from simple regurgitation in that the raised food is expectorated in the latter disease, but is swal- lowed again in the former. The ascent of the food from the stomach causes a pleasurable sensation to these patients, and they assist the act by bringing into effect the pressure of their abdominal muscles. In severe cases the rumination occurs after every meal, and lasts either only for the first hour or for five or six hours. The condition of the secretory function is variable. Jurgensen found no free HC 1 , Bear and Boas found subacidity, while Alt demonstrated hyperacidity in one of his cases. In some patients secretion was found to be normal. In three of such cases I ob- served that the state of the secretion varied, as expressed in the chemical analysis of the raised masses according to the time after the ingestion in which they were regurgitated, and the com- bining power for HC 1 which the particular food possessed. If they were regurgitated immediately after the meal, they were faintly acid or neutral, contained no free HC 1 nor ferments, which, however, were present within forty-five minutes of the first ingestion of food. It is probable that many of the discrepancies concerning the state of SYMPTOMS OF RUMINATION. 769 the secretion, as stated by the various authors mentioned, can be ex- plained on the same grounds. Alt has suggested a very interesting theory in explanation of the ruminating habit (“ Berlin, klin. Woch- enschr.,” Bd. lxxxviii, Nos. 26 and 27) : he suggests that the object of the act may be the correction of defective chewing and insaliva- tion of the food, and the hyperacidity caused thereby. Acting ac- cordingly, Alt treated his patient with alkalies, and claims to have found that the case ruminated less frequently and by and by could suppress the habit. Boas (“ Berlin, klin. Wochenschr., ” 1886, No. 831) has published a case of rumination with subacidity, and in this case improvement followed the administration of HC 1 . Ac- cording to Einhorn, but 106 cases of this malady have been described up to 1896, which cases occurred chiefly among the pro- fessional and educated classes — physicians, lawyers, and philolo- gists. This observation was also made in a report by Johannessen (“ Zeitschr. f. klin. Med.,” Bd. x, S. 274). The following is a brief account of a case occurring in my private practice : A. F., aged thirty-eight, mother has been a highly nervous woman, much afflicted with insomnia and neuralgia ; father died at the age of fifty-six from Bright’s disease. He was a very irascible and eccentric man. A. F. has had no severe disease, except gout four years ago. He is a pianist of exceptional ability, and has played in foreign countries as well as in the larger cities of the United States. Ordinarily and when in a quiet frame of mind he rarely ruminates, but when he gives instruction, particularly when he has to perform at a concert, or at other times when he is emotionally excited or disturbed, he begins to raise food into his mouth, which he at first swallows for about two hours. He confesses that he chews the food, and actually enjoys it, but at the expiration of two hours the muscles of mastication become so exhausted that he can no longer chew the raised masses. He would then like to put an end to the ruminating, or rather to the rising of the food, but then can not stop it, as it persists in coming up from his stomach. He then terminates the rumina- tion by voluntarily evacuating his stomach through vomiting, which he accom- plishes very easily. The masses begin to ascend within ten to fifteen minutes after a meal, and are then very faintly acid. He is also aware that they begin to taste salty sour, as he calls it, forty-five minutes to an hour after the meal. The total acidity one hour and a quarter after a meal, as judged from the regurgitated masses, is 70; free HC 1 30. Erythrodextrin present; achroodextrin present. Gas- tric' motility, as determined by Hemmeter’s method, is evidently exaggerated. Physical examination of the thoracic and abdominal organs negative. Urine negative. Examination of blood negative. On one occasion this patient had not ruminated for three weeks, when the time came for him to fulfil an engage- ment at a concert. The author, for the sake of study, was present when he took his supper on the evening of this concert. Within fifteen minutes after the supper we observed, by the movements of his throat, he had begun his old 7;o NEUROSES OF THE STOMACH. bad habit, which kept up during the entire evening, and was plainly observable while he was performing at the piano during the concert. Atony and dilation may be present, together with rumination, and the state of the motility seems to vary as much as that of secretion. The general nutrition is not, as a rule, affected, although the disease may have existed a long time ; but when the patients persistently spit out the ascending masses of food, instead of swal- lowing them again, or when severe disturbances of secretion and motility exist, the patients rapidly lose strength and weight. According to von Hacker and G. Singer, an insufficiency of the cardia, and a dilation of the esophagus immediately above the cardia, may be caused by mechanical expansion, resulting from the regurgitation of large bits of food. This esophageal expansion has been demonstrated by these authors with the esophagoscope. Prognosis. — This is not a serious disease, as the general nutri- tion remains good, and if the patient really does begin to suffer, he may be relieved by a rational psychical and symptomatic treatment, particularly if the patient himself will aid the therapeutic measures by self-control. The diagnosis presents no difficulties whenever the physician can observe a patient in the act of rumination ; regurgi- tation and emesis imply the spitting out of food, and are always associated with nausea or some other unpleasant sensation. Treatment. — Medicinal treatment in this disease is of little value. The state of the secretions should be carefully determined, and subacidity or achylia corrected by the administration of HC1, and hyperchylia by the use of calcined magnesia and bicarbonate of sodium. Korner is enthusiastic on the value of small pieces of ice given directly after meals. The stomach-tube has been used for the lavage and artificial feeding, but the relief has been only temporary. The physician should, however, in all cases insist on slow eating and careful chewing; the food should be easily digest- ible and largely composed of gruels and diet of a soft consistency. The patient should always take his meals in the presence of persons for whom he has considerable respect, and who understand to op- pose the morbid habit with kindness and yet with emphatic per- sistence. The success of the treatment will depend upon the will- power of the patient himself. Whenever the patient feels a desire to ruminate, he should be prompted to resist the temptation with all the self-control at his command. He should be guarded against using the contraction of the abdominal muscles to assist the act. INSUFFICIENCY OF THE PYLORUS. 77 1 Ponsgen, Boas, and Einhorn report permanent cures resulting from such persistent autosuppression. A trial might be made with the intragastric use of the faradic and galvanic currents. Hydropathic methods are sometimes useful. In one case observed by myself, in which every meal was persistently ruminated, I carried out rectal alimentation for twelve days, not allowing anything to enter the stomach during this time. Since then nearly two years have elapsed and rumination has not thus far returned. I hesitate in attributing this recovery to the rectal alimentation, although, of course, it was impossible for the patient to regurgitate and ruminate when no food was contained in the stomach. However, the psychical effect of hospital treatment, the entirely new surroundings, and attendance by intelligent nurses, the constant rest in bed, may have contributed as much as the rectal feeding toward the re- covery. In another case the author cured the patient by giving ten grains of quinin after each meal. The good result is not at- tributed to the antimalarial effect, but rather to the fact that the quinin rendered the food so disgustingly bitter that the patient suppressed the regurgitation. Rossier claims to have cured one case by muriate of morphin, and another by large doses of opium. In my experience these remedies have been useless. INSUFFICIENCY OR INCONTINENCE OF THE PYLORUS. It has been known for a long time that an insufficiency or incon- tinence of the pylorus may be caused by organic diseases of the stomach and intestines, by carcinoma and ulcer, by bringing about a partial or complete obliteration or carcinomatous infiltration of the annular muscle, so that the latter becomes incapable of function- ing ; or it may be caused by a stenosis of the duodenum leading to advanced dilation of the initial part of the same. Attention was first called by Ebstein to those interesting, though very rare, cases of insufficiency, which appear, in the absence of ana- tomical changes, genuine neuroses — paralysis of the motor nerves of the annular muscle. It had been previously observed by Ebstein as a concomitant phenomenon of myelitis due to compres- sion, and also in hysteria and gout; but it may, perhaps, occur also as an idiopathic malady. If the muscular insufficiency is con- fined to the pylorus, then the foods and liquids, according to the degree of the insufficiency, either remain a very much shorter time than usual in the stomach, or enter the intestines immediately 772 NEUROSES OF THE STOMACH. after their ingestion. The nutriments then are not at all digested in the stomach, or only to a slight degree, so that the whole, or almost the whole, burden of digestion falls upon the intestine. Since, however, repeated experiments upon human beings and animals have proved that the intestine, in normal conditions, may entirely make up for the lack -of digestion in the stomach — and the experience gained from the treatment of persons that have undergone a resection of the pylorus confirms this ; therefore even with protracted duration of the pyloric insufficiency disturbances of nutrition generally fail to appear, especially when an easily digestible diet is prescribed, suitable to the malady, and provided that the intestinal functions are normal. The symptoms of pyloric insufficiency are, in brief, the following — viz. : If frequent vomiting and belching existed, these suddenly cease after the setting in of the insufficiency. If rather large particles of food get into the intestine which mechanically irritate its mucous membrane more than usual, then the increased peristalsis may cause diarrhea. This may also be brought about by very cold or very hot foods or drinks, which are gradually warmed or cooled by the stomach, as the case may be, before their entrance into the intes- tine, when the closure of the pylorus is normal. If a quantity of air was swallowed with the foods, or if drinks rich in carbonic acid have been imbibed (beer, seltzer water, champagne), a very acute tympanites of the intestine may develop from the escape of air or carbonic acid gas. According to Ebstein, one can not succeed in distending the stomach with the artificial production of carbon dioxid in the organ by acid, tartrate and sod. bicarb., one teaspoonful of each in 4 ounces of water in separate tumblers ; but Ewald, Boas, and other authors justly contend that this evidence is not conclusive; since, even when the musculature of the pylorus functions in a normal manner, every attempt at distending the stomach by means of gases may remain unsuccessful, because the amount of the gases formed is too small. Further, with an empty stomach the pylorus (Kussmaul) is normally so relaxed that a portion of the carbonic acid gas may easily pass over into the intestine, without the pres- ence of any real insufficiency. This source of error may, however, be removed by letting the patient eat a test-breakfast before the distention of the stomach (Fleischer), since then, under normal cir- cumstances, the closure of the pylorus becomes so firm that the carbonic acid gas set free can not at once escape into the intestine ; INSUFFICIENCY OF THE PYLORUS. 773 or if, instead of C 0 2 , air is forced into the stomach by means of a tube and a pump, increasing the supply according to necessity. If the air passes quickly into the intestine, the inflated ascending colon appears as a thick swelling on the right side of the abdomen. For a proof of the purely nervous origin of insufficiency it is necessary to exclude the above-mentioned diseases of the stomach and intes- tine, and such organic diseases of the stomach as chronic gastritis, which probably bring about a serous infiltration of the annular muscle, and may lead to a temporary insufficiency (Eichhorst, Boas). If the insufficiency be due to a stenosis of the duodenum, the stomach may very well be distended by C 0 2 or air, in spite of insufficiency. If, after finding out the lower limits of the stomach, quantities of water are introduced through the tube, and no dullness appears in the lower parts, while gurgling noises, before lacking, now become audible in the intestine, and if the intestinal loops, just before this, gave a tympanitic resonance, and after the intro- duction of water exhibit a muffled sound, insufficiency is to be inferred. It has been claimed that after the introduction of one grain of salol or o.i gr. of iodoform with the test-breakfast, sali- cyluric acid can be shown in the urine after taking the former, and iodin in the saliva after taking iodoform, much sooner than with continence of the pylorus, as these chemicals enter more quickly into the intestine, and on account of the neutralization of the hydrochloric acid by the alkaline intestinal juice, they are immediately converted into soluble compounds which may be absorbed. I have explained the fallacy of these tests. Insufficiency of the pylorus may be recognized by the author’s method of intubating the duodenum (“ Archiv f. Verdauungskrank- heit.,” Bd. n, S. 85), and by the spiral revolving sound of F. Kuhn, of Giessen, and of F. B. Turck, either of which may be used for sounding the pylorus. This operation was first performed by the author and also by Dr. F. B. Turck, and Kuhn’s claims of priority of sounding the pylorus are unfounded (Hemmeter, “ Die Prioritat d. Pylorus-Sonderung,” “ Centralblatt f. innere Medicin,” 1897, No. 2). The interesting observation of a case of insufficiency, reported by Schiitz, in which it was possible to distend the stomach by means of C 0 2 but not by air, so that by the increased irritation of the mucous membrane of the pylorus by the carbonic acid gas a contraction of the annular muscle was brought about, but with the forcing in of air the stomach did not become distended, points to the fact that different degrees of insufficiency occur. If, 5i 774 NEUROSES OF THE STOMACH. as easily happens in a case of pyloric insufficiency, some of the contents of the intestine go back into the stomach, causing dys- peptic complaints by the irritation of the mucous membrane and neutralization of the HC 1 , this can be recognized by testing for bile. Therapeutics. — If symptoms of irritation of the intestine — namely, diarrhea — are absent, only dietetic treatment is necessary. In order to relieve the intestine of its excessively burdensome task, we must prescribe easily digestible, well-prepared foods, which are to be carefully masticated, and are not to be taken too hot or too cold. If, on the other hand, complaints such as diarrhea appear, we must attempt, in addition to the treatment of the causal disease, to get rid of the insufficiency by means of massage, internal and ex- ternal galvanization and faradization applied directly to the pylorus by the author’s method (a spiral electrode contained within a rubber tube, and, after introduction, brought into contact with the pylorus, as demonstrated by X-rays), douches, and eventually also by giving strychnin, gr. 3V, t - K If flatulence and constipation arise on account of suppression or loss of hydrochloric acid secre- tion, which, as is well known, has a stimulating effect upon the peristalsis of the intestine, and, further, acts as an antiseptic, then the massage, as well as the galvanization, is to be applied also to the intestine, and dilute HC 1 should be administered in doses of 30 drops largely diluted and taken after meals through a tube or the double Aaron capsules. In all other indications the treatment must be directed to the cause. ATONY OF THE STOMACH (Myasthenia Gastrica; Mechanical Insufficiency of the Stomach). In the consideration of dilation of the stomach we have fully quoted the classifications of Riegel, Schreiber, Boas, Naunyn, and Rosenbach. By simple atony we mean that combination of symp- toms in which there exists a disproportion between the peristaltic work the stomach has to perform and its real expelling muscular force. Objectively, the disease makes itself known by the fact that the ingesta are retained in the stomach beyond the normal time, but although the muscular action of the organ is weakened, the food is eventually expelled into the duodenum. By this it is distinguished from the mechanical insufficiency of the second ATONY OF THE STOMACH. 775 degree, the pronounced dilation, in which the food is, as a rule, per- manently retained in the stomach, and only exceptionally reaches the bowels. Every relaxation of the muscular wall that is not due to any pyloric or other mechanical obstruction may be justly designated as an atony. In simple atony the stomach is not considerably enlarged in the empty state, but only becomes so with increasing burdening of the ingesta, but in atonic dilation the diseased organ remains in a dilated state even after it is empty, (i) This disease may occur as a typical, primary, idiopathic neurosis, as a consequence of per- sistent overloading of the stomach with indigestible food, particu- larly with liquids. It may appear very suddenly as a transient affec- tion, under the influence of violent emotional disturbances, — fright, anger, grief, etc., — occurring in this way principally in neurasthenic persons. It is probable that gastric myasthenia may be inherited, and may be transmitted through several generations. It is gener- ally referred to as the so-called “ weak stomach ” in some families. The abuse of alcoholic liquors, particularly of beer, and even of coffee and soups, has been assigned as a cause. (2) Myasthenia occasionally appears as a reflex neurosis evolved from other dis- eased organs — for instance, diseases of the liver, bile passages, peritoneum, intestines, kidney, and sexual apparatus. (3) It occurs as a secondary neurosis, constituting part of the symptoms of hys- teria, neurasthenia, gastrospasm, cardiospasm, and pylorospasm. It has been observed as a complication of gastroptosis, nervous dyspepsia, ulcer, and chronic gastritis. There are a number of intestinal affections which may be complicated with, or even cause, atony. These are stenosis in the inferior horizontal portion of the duodenum, or stenosis of the jejunum, enteroptosis, and stenosis of the colon ; passive congestions and enlargements of the liver and cholelithiasis are definitely known to be etiological factors. Criti- cally speaking, we designate only such cases gastric atony in which the organ retains its normal size when it is empty. As soon as the stomach remains permanently enlarged, even when it is empty, it is more logically classed with the motor insufficiency of the second degree, as atonic dilation. As we have seen in the section referred to, Riegel makes a separate class for stenotic dilation. The final cause of simple atony, or myasthenia, is malnutrition, overstretching of the muscles and motor nerves of the stomach, or an early and progressed exhaustion after undue and improper ex- ertion. Occasionally unknown neurotrophic influences may be re- sponsible for the origin of atony. As secretion and absorption depend 776 NEUROSES OF THE STOMACH. more or less upon energetic contraction of the gastric muscularis, they are in most cases interfered with in the absence of effective muscular tonicity. The gastric contents do not diminish in quantity as rapidly as they should, and in consequence of this the gastric wall is excessively expanded by the prolonged weight of food. If fermentation of the ingesta occurs with abundant formation of gases, the expansion will be still greater. The gaseous distention may secondarily produce spasm of the pylorus and cardia, thus adding another etiological factor to the causation. If the atony is very far advanced and has persisted for a long time, it may develop into an irreparable dilation, particularly if dietetic and hygienic regula- tions are disregarded. We have observed a number of cases of this kind, in which permanent dilation was developed when long- standing gastric distress was left unheeded. Myasthenia — by diagnostic methods for judging the motility — may be found to be very pronounced, and still remain latent and unnoticed even by the patient for a long time. The following is an example of this class of cases : Miss S., aged twenty-two, a well-built and apparently healthy girl, moving in the best circles of social life, complains of only one symptom, that is a severe headache, occurring two or three times of every week, and lasting for twenty -four hours. On being questioned about her stomach, she asserts that her digestion is good, appetite excellent, and bowels regular. She eats all kinds of food apparently without distress. On passing the tube in the morn- ing, on an empty stomach, 200 c.c. of a slightly yellowish mucous liquid were obtained which shows free HC 1 by Congo paper. The next day she was directed to take the double test-meal. One hour after the second meal the contents were drawn, and rice and egg of the early breakfast, which was taken six and a half hours before, were still present in her stomach, together with a considerable amount of mucus. Total acidity, 60 ; free HC 1 , 20. Subse- quently the same state of affairs was found after other test-meals. Peristole by author’s method decidedly impaired. The striking feature of this case is that, although there was a pro- nounced gastric atony, the patient was not at all conscious of it, and regularly expressed surprise when she recognized food in the lavage that had been taken eight to twelve hours before. It is very prob- able that such cases as this one would develop the unmistakable symptoms of myasthenia in a very short time if left untreated. The author examined 100 members out of a medical class of 140 stu- dents ; of these, five had gastric atony and were unaware of it. Superacidity and supersecretion may cause cardiospasm and pylorospasm, and subsequently gastric atony, by the irritation SYMPTOMS OF GASTRIC ATONY. 777 of the muscular structures of the orifices. But, reversely, gastric atony may cause superacidity and supersecretion by the fact that the ingesta are retained in the stomach for an unduly long period, and thereby excite the gastric glands to stronger functioning. Stiller and Boas assert that gastric atony rarely develops into per- manent gastric dilation. The subjective symptoms of gastric atony are very similar to those of gastritis and incipient dilation. The patients complain of pressure and pain in the head, the feeling of pressure and distention in the stomach, a premature sensation of fullness during eating by which the appetite becomes appeased very rapidly, very frequent eructation, and persistent constipation. The feeling of pressure is intimately associated with the ingestion of food. When the stomach is empty, the patient feels quite well. The headache is very frequently observed, together with the so-called stomach vertigo. We agree with Boas that this so- called gastric vertigo (Trousseau, “ Gazette des Hopitaux,” 1862) is much more frequently found in atony and dilation than in any other gastric disease. The feeling of pressure and distention may persist as long as there is food in the stomach : in recent cases, about one hour; in advanced cases, it continues from one meal to the other. One of the most frequent symptoms is eructation of air, which generally has the taste of the food that has been last taken. We have noticed that the most annoying sensations of pressure in the advanced cases are felt after breakfast, at a time when one would presume that they should be absent, since the stomach should have been rested during the night. The duration of the time after meals during which the eructations continue is generally a good indica- tion of the extent and degree of the myasthenia. In some cases, however, we may be confronted with typical neurotic regurgitation and eructation, that has existed before the atony developed, and then this indication is invalid. If there is hyperacidity, the atony may be associated with attacks of vomiting, and pyrosis is gener- ally present. The constipation is undoubtedly an expression of the general atony of the entire gastro-intestinal tract. Objective Symptoms. — The most important distinguishing sign between simple atony and dilation consists in the fact that the stomach, in the former, should be empty in the morning, when nothing has been taken since the previous supper; in other words, the jejune stomach of atony contains no food particles, while the stomach in a state of dilation does contain them. The splashing sound in the epigastric region is absent in the morning with simple 77 8 NEUROSES OF THE STOMACH. atony, but it is present in dilation. The size and location of the stomach vary physiologically. A myasthenic stomach yields and distends with greater readiness when it is filled with water or air than a normal stomach. Boas asserts that even an atonic stomach may react more normally to the distending force of water and air in such cases in which the superimposed layers are swelled and much thickened by inflammatory infiltration. The methods of in- vestigation and diagnosis which we have found useful are, in addi- tion to inspection, palpation, percussion, and auscultation, the dis- tention of the stomach by air or carbon dioxid gas, the Hemmeter intragastric stomach-shaped bag, and the gastrodiaphane. Very frequently the contour of the greater curvature may be recog- nized on the outside of the abdomen. Palpation may, in some cases, instruct us concerning the limits of the organ, and enable us to separate it from adjacent organs. The so-called splashing sound may be elicited by permitting the patient to drink a glass of water, and then, placing the palm of the left hand firmly over the right hypochondriac region, and by gently tapping the epigastrium with the right hand, the sound is generally very evident if atony is present. In most cases of gastric atony a splashing sound can be heard with binaural stethoscope on shaking the stomach from the outside. Dehio has given a very expedient method for judging the elasticity of the gastric walls by means of gradually increasing quantities of water : at first ^ of a liter is taken, and the location of the greater curvature determined ; then, in short intervals, of a liter is taken at three successive periods, and after each ^ of a liter increment the further descent of the greater curvature is de- termined by palpation and percussion, and the niveau of the water in the stomach ascertained by holding the funnel against the ab- dominal wall and observing the level at which water either flows into or out of the organ. A healthy stomach will not reach the line of the umbilicus under these conditions, while an atonic stomach may have transgressed far beyond it. Auscultation elicits sounds only when the stomach contains liquids or shortly after they are ingested. It is best to use the binaural stethoscope in these cases, as then both hands are free to palpate and move the stomach to obtain the percussion-sound. Boas holds that we have no reliable method to test the gastric elasticity and tonicity (/. c., p. 76). We consider that our method of recording the gastric peristalsis on the kymograph, as described in the first part of this book, is also an excellent method for investigating the gastric SYMPTOMS OF GASTRIC ATONY. 779 tonicity, for, as our stomach-shaped intragastric bag on being dis- tended gradually fills out the lumen of the stomach exactly, the indications of pressure which are obtained on the kymograph are reliable representations of the tonicity. Moreover, we have experi- mented with an electrodiaphane contained within our stomach-bag, so that when the bag was distended in a dark room, the gradual descent of the greater curvature could very plainly be seen. By reference to the description of the apparatus on pages 76 to 78, it will become evident that we can easily determine the amount of air or water with which the bag is distended within the stomach ; so with this method, which in a modified form was also used inde- pendently, after our first publication, by Professor Moritz, of Munich, for studying the gastric motility, we may determine also the elasticity and tonicity of the stomach. Percussion . — In percussion of the stomach we must attempt to define its four limits — viz., the upper, lower, right, and left limits. The lower limit may, on percussion, be confounded with the trans- verse colon if the latter still be in its normal position. The way out of this difficulty is to fill the transverse colon with water, which gives a dull percussion-note through the abdominal wall, while the stomach may be distended with air or gas, giving a clear tympanitic sound. When both the stomach and the colon are filled with gas or with solid material simultaneously, it is almost impossible to dis- tinguish between the two by percussion. It is best to evacuate the colon and fill the stomach with water, or vice versa to evacuate the stomach and fill the colon with water. In our clinic we use the rubber stomach-shaped intragastric bag methodically, and when it is distended, there is no difficulty at all to percuss and palpate the stomach. The determination of the upper border of the stomach is, in our experience, no easy matter, since there are no very striking differences in the percussion-note of the lower edge of the left lung and the highest portion of the gastric fundus which is nor- mally covered over anteriorly by the lung in inspiration. The upper border may be best determined by filling the stomach with water and then percussing over the left lung along the parasternal line from above downward. Pacanowski ( “ Deutsche Arch. f. klin. Medicin,” Bd. XL, S. 342) gives the following determinations of the upper limit of the stomach : In the left parasternal line it is at the lower edge of the fifth rib or in the fifth intercostal space. In the left mammillary line the limit is in the fifth intercostal space extend- ing to the sixth rib, or into the seventh rib. In the anterior left NEUROSES OF THE STOMACH. 780 axillary line the upper limit is at the lower edge of the seventh or eighth rib, rarely under the eighth rib. The determination of the left and right gastric limits seems most impractical to us, and not of diagnostic value, because here we may confound the percussion- notes of organs superimposed upon the stomach. In our experience a clear conception of the size and location of a normal stomach can be obtained only when it is distended by gas, air, or water. Naturally, this can not be done if there is suspicion of recent ulcer or perigastritis. In such cases we now coat the inside of the stomach with bismuth subnitrate with a gastric powder-blower, and observe the size of the organ by means of the X- rays and skiagraph — the rays being cut off by the bismuth. The powder can readily be blown in through an ordinary soft stomach-tube. We have already spoken of the value of the elec- trodiaphane in ascertaining the size and location of the stomach, and, notwithstanding numerous objections, consider the method practical. After all, the most convenient method of determining gastric atony, and that which is available for every practitioner, is by means of the double test-meal used in our clinics. (See pp. 120 and 121.) According to Boas’ suggestion, a full meal is preferably given in the evening, when a healthy stomach will show no demonstrable signs of food particles the next morning. It should not be forgot- ten, in this connection, that even healthy stomachs may contain mucus, gastric juice, and bile in the morning before food is taken. The chemical analysis of the stomach-contents in gastric atony yields no results useful for diagnosis, because the state of the secretion varies considerably according to the degree of the mechanical insufficiency. In the primary stages of gastric atony superacidity is, as a rule, present; at other times the secretions may be normal, and, in the latter stage, we may have subacidity or even achylia. The drawn stomach-contents in atony, on settling in a glass vessel, do not show the three characteristic layers of solid, liquid, and froth which are usually found in the drawn con- tents of the dilated stomach. We have never observed processes of fermentation in simple atony. The secretion of pepsin and ren- nin is generally found to be proportionate to the secretion of HG 1 . Thirst is normal, and the amount of urine passed is not reduced. Disturbances in nutrition may gradually develop if the diet is inap- propriate or if the patient refuse to eat sufficiently for fear of causing gastric distress. TREATMENT OF ATONY. 7 8i The course of gastric atony is a chronic one, and the symptoms are subject to many deviations. Stiller and Boas hold that gastric atony comparatively rarely develops into dilation. Notwithstand- ing this, the disease generally produces considerable systemic weakness. A variety of nervous disturbances accompany the malady. Prognosis. — In recent cases the prognosis is favorable, provided that they are systematically treated and the fundamental causatives of the disease can be removed ; but in pronounced atony, and that of long standing, complete recovery is rare. Diagnosis. — Gastric atony and myasthenia may be confounded with chronic gastritis, nervous dyspepsia, dilation, and megalogas- tria. In chronic gastritis the stomach is not enlarged, as a rule, since the motility is good ; excess of mucus is common in gastritis and rare in atony ; but as atony may predispose to gastritis, the two affections may sometimes exist side by side. Nervous dyspepsia is characterized by a great deviation and uncertainty in the symp- toms ; even the motility may be at times seemingly much affected, but at others, if the case be strictly watched, the motility will be found to be perfect. In nervous dyspepsia there are painful points in the district supplied by the great abdominal sympathetic plexuses — the celiac, solar, and hypogastric. The painful spots are rare in simple atony. Nervous dyspepsia and atony may exist simulta- neously, and one may cause the other; in such cases it will be diffi- cult to determine which is the primary disease. The differential diagnosis between dilation and simple atony should present no difficulties when modern methods of determining the size and capac- ity and motility of the stomach are used (pp. 98 to 1 12); neither should there be any difficulty in distinguishing atony from megalo- gastria, since the latter is not a disease, but simply a condition of big stomach, which performs its functions normally. Treatment. — The most important part of the management of gastric atony is prophylaxis, which includes the avoidances of all known causes of the affection : defective teeth, irregular mode of life, hasty eating, and abnormal burdening of the stomach with food and drink, constipation, as well as the frequent abuse of purgatives. Even when the distinct cause of the malady is not known, one will do best to prevent the full development of myas- thenia by rational dietetic and hygienic treatment before functional disturbances become manifest. We have already remarked that atony may be inherited. Whenever this is noticed, such persons 782 NEUROSES OF THE STOMACH. should be particularly guarded and careful in the selection ol their diet. There are a number of constitutional diseases which, in our experience, undoubtedly predispose to this state. These are tuberculosis, syphilis, anemia, chlorosis, and cholelithiasis. It is present also after exhaustive hemorrhages, and is particularly ominous when the condition occurs after hemorrhages from gastric ulcer. Typhoid fever has, in our experience, frequently been followed by gastric atony ; the same is true of infectious diseases generally, particularly scarlet fever, malaria, diphtheria, and influenza. We have also noticed gastric atony follow a number of operations for abdominal tumors, and particularly ovarian neoplasms. It is very probable that the relaxation of the gastric walls is here largely due to mechanical causes, similar to that which occurs after very fre- quent and rapidly consecutive pregnancies. In all of these instances the abdominal walls do not regain their tonicity. We have described this condition fully in the section on Gastroptosis. Prophylaxis consists in appropriate hygienic living, much sleep (at least nine hours in the twenty-four), and strengthening of the abdominal mus- cles — the latter is one of the most important elements, not only in prophylaxis, but also in the treatment of atony. The training of the abdominal muscles should be carried out according to rules laid down in Illoway’s work on “ Constipation,” and Sandow’s book on physical culture. The treatment proper of a fully developed atony must have regard for the fundamental cause — for instance, in syphilis specific treatment will be the only proper course to pur- sue; in anemia we must have recourse to preparations of iron which have no direct deleterious effect upon the mucosa. Among these preparations we prefer the iron albuminates and peptonates, also ferratin and extract of bone-marrow. With pronounced enteroptosis, particularly in women, abdominal gymnastics can not be effectively carried out, on account of the great exhaustion of the patient. In some cases of this type palliative results may be obtained by abdominal massage, faradization of the abdominal muscles, baths, and, last but not least, a well-fitting abdominal bandage. In a few cases it will not be possible to trace any cause whatever, though even in these it is well to carefully study the alimentary tract itself before giving up the hope of determining the etiology. The most important factors of direct treatment are : (1) diet, (2) hydriatic, (3) electric procedures, (4) massage, and (5) medicines. The prin- DIETETIC MANAGEMENT OF ATONY. 783 ciple underlying the diet in gastric atony is that of frequent and very small meals, which, although quite nutritious and digestible, must not be voluminous. The diet should, as a rule, consist of fats, carbohydrates, and proteids, mixed. If there is an excess of HC1, there is no objection to increasing the proteid food, but in doing so it is well to watch the ratio of the ethereal to the combined sulphates, and the indican in the urine. If the ratio of the pre- formed to the combined sulphates is very high, and there is an excess of indigo in the urine, it is, in our experience, worth the trial of adding more fats and artificially prepared amylaceous foods, such as dextrinized flours, etc., for it has been found that the general symptoms, as well as the aforementioned indications in the urine (in rare instances, in which proteid diet does not agree in hyper- acidity), will improve if the proteids are cut down and the other food substances increased. Together with this diet in hyper- acidity the use of alkalies, magnesia usta, sodium bicarbonate, etc., and of ptyalin, or of malt or taka-diastase, is sometimes service- able. The diet which we recommend for gastric atony is the fol- lowing : 8 A. m. — 250 gm. of bouillon, oatmeal, or 100 gm. of milk and 100 gm. of tea or coffee. 10 a. m. — One soft-boiled egg, or 70 gm. of finely scraped tenderloin, either raw or broiled, and 20 gm. of toast. 12 m. — A broiled sweetbread, or 150 gm. of broiled oysters, or little-neck clams, or 100 gm. of finely scraped beef slightly fried in butter; 200 gm. of potato puree, and, if hyperacidity is present, we give half a wineglassful of some reliable malt extract. 3 p. m. — 200 gm. of Mosquera’s beef chocolate (P., D. & Co.). 6.30 p. m. — 60 gm. of scraped raw ham, or the same amount of fried perch or carp ; 50 gm. of toast, and 30 gm. of butter. 10 p. m. — 100 gm. of some approved light Moselle wine. This list calls for six small meals in the day, and is modeled after those recommended in European text-books. We have found that very frequently the atonic stomach is unable to evacuate one meal before another is taken. This danger should be studiously avoided, and if detected, it is best to allow only two meals a day — a breakfast and a late dinner — according to principles laid down in the chapter on the Use and Abuse of Rest, etc. In the section on Dietetics we have given other diet-lists suitable for this affection. A number of competent authors consider the treatment of atony and a chronic dilation together in the same 7§ 4 NEUROSES OF THE STOMACH. chapter. Personally, we draw a very sharp distinction between these two affections and their treatment. The therapy of dilation is considered in the chapter devoted to this subject. The total quantity of liquids should be limited to I y 2 liters a day. This includes the soups, coffee, tea, milk, alcoholic beverages, and water. Alcohol, except in the quantities suggested in the diet- list, should not be allowed. Purgatives and narcotics are forbidden. If the thirst is intense, which, however, is rarely the case, water may be introduced by enema. When milk is well digested, and no idiosyncrasy exists against it, so-called milk cures may have a bene- ficial effect. There is no doubt that an exclusive milk diet insures rest and is very sparing upon the stomach, but it is a two-edged sword. We have seen cases in which the atony undeniably became aggravated by the milk diet. The diet must vary also with the amount of HC 1 secreted. With increased secretion of HC 1 the meats may be permitted to prevail. All meats should be run through the meat-chopper. Eggs in all forms are permissible in this state. When the secretion of HC 1 is diminished, we permit the use of spin- ach, carrots, beans, cauliflower, and asparagus. All vegetables should be cooked and given in the form of purees ; among these are the potato, rice, sago, pea, and bean puree. The use of beer should be forbidden or very greatly limited ; we do not, as a rule, forbid small doses of good wine. Where good wine can not be obtained, it is safest not to prescribe wine of a doubtful quality, but to order dilute whisky or brandy. Constipation should be met with proper diet, and medicines should not be used unless they are positively unavoidable. We have already spoken of the diet best suited for constipation. In very stubborn and pro- tracted cases glycerin suppositories and water injections will be more effective than medicines given by the mouth. (See Illoway on “ Constipation,” and E. A. Ewald, “ Ueber d. habituelle Obsti- pation u. ihre Behandlung,” 1897.) An advantage is gained by going to stool at a definite hour. There are cases, however, in which a natural stool that occurs every two or even every three days spontaneously is much better, and will do more toward gradual recovery from the evil of constipation than a stool pro- duced artificially every day. Where the patient insists on medi- cine, and it is really unavoidable, aloes, strychnin, and cascara sagrada are most favored by the author. (The syrup cascara, “ active,” Clinton Pharm. Company, and the elixir and fluid ex- tract of cascara sagrada, P., D. & Co., or S. & D., can be safely MASSAGE AND MEDICINAL TREATMENT. 785 recommended.) Podophyllin in the form of pills is a proper medi- cation. The following formula is the one which we favor: IJ . Podophyllin, 0.26 gr. iv Strychnin, sulphate, 0.2 gr. Glycyrrhizoe, q. s. F. pil. No. xii. M. SlG. — One pill before supper and one at bedtime. Dose increased to two pills the next day if necessary. The compound extract of rhubarb is also an effective combi- nation ; but calomel, colocynth, jalap, and scammony, and the very concentrated purgative waters, such as the Hunyadi Janos, the Rubinat-Condal, aftd Veronica, must be avoided if possible. Boas, in contrast to other authors, states that lavage is not only unneces- sary, but harmful in simple atony, because stagnation does not occur in this disease and there is therefore no necessity for washing out the stomach. I employ lavage, however, not to combat any pre- sumable stagnation, but as a sort of intragasjtric hydropathic mas- sage. For this purpose I use an intragastric douche with hot and cold water alternating. The instrument devised by F. B. Turck is useful for this purpose. The electrical treatment with which Einhorn has achieved remarkable results is undeniably a valuable means of therapeusis in this affection. It may be applied externally with large felt-covered plates applied to the abdomen directly, or by the intragastric electrode. We usually apply the current fifteen minutes and repeat it daily for three weeks. Massage should be applied, not only to the stomach, but to the entire abdomen. The method of application (concerning abdominal massage, see Illoway on “ Constipation Hoffa, “ Technik d. Massage,” Stuttgart, Enke, 1893, also Penzoldt and Stintzing, “ Handbuch,” Bd. iv, S. 34-39) is described on pages 290-299. Treatment by Medicines . — The only drug which one may depend on for improving the gastric tonicity is strychnin. When atony is accompanied with suppression of gastric juice and anacidity, we can practically associate it with HC1 and gentian in the following manner : J& • Strychnin sulphate, 0.02 gr. ^ Dil. hydrochloric acid, . ......15.6 f 3 iv Elixir of gentian, q. s. 180.0 f^vj. M. SlG. — One- half of an ounce in two ounces of water, after meals, through a glass tube, three times a day. 786 NEUROSES OF THE STOMACH. When there is excess of HC 1 , it is well to combine the strychnin in the following manner: Strychnin sulphate, g r - A Bismuth salicylate, • 7-5 3 b Sodium bicarbonate, • 1125 3 ^ Magnes. ustae, . 4.0 3 i Peppermint water enough to make . . 180.0 Z v i- Sig. — A tablespoonful in a wineglassful of water after each meal t. i. d. Creosote has been recommended by Klemperer (“ Berlin, klin. Wochenschr.,” 1889, No. n) and A. Pick (“Vorl. fiber Magen- u. Darmkrankh.,” 1895), but Fleischer has found that the motility is still more reduced under creasote, and in the author’s experience it proved useless. Ergotin, which is recommended by Leube, is, in my opinion, a dpubtful remedy for this purpose. Ichthyol has been claimed by Pick to benefit atony, particularly when it is asso- ciated with fermentative processes in the bowel. In severe cases of gastric atony with recurrent gastric distress we have had very gratifying results by rectal feeding for from six to eight days, and total exclusion of food from the stomach : that is, we treated the atony as we would treat a severe gastric ulcer. The good results were permanent. During the period of rectal feeding the patient must remain in bed. LITERATURE ON NERVOUS DISEASES OF THE STOMACH. 1. Adler and Stern, “ Berl. klin. Wochenschr.,” 1889, Nr. 33 - 2. Alt, Konrad, “ Ueber das Bestehen von Neurosen und. Psychosen auf dem Boden von chronischen Magenkrankheiten,” “ Archiv f. Psychiatrie u. Nervenkrankheiten,” Bd. xxiv, 1892. 3. Alvermann, “ Die nervose peristaltische Unruhe des Magens und Darms,” Dissert., Bonn, i895~’96. 4. Arany, S. A., “ Ueber Dyspepsia nervosa und was als solche diagnosticirt wird,” “Ungar. med. Presse,” 1898, in, 706-711. 5. Bamberger, “ Tetanie bei Magendilatation,” Bericht der “Contracture Mortelle d’Origine Gastrique,” “ Gaz. Hebdom.,” 1889. 6. Bentejac, “These de Paris,” 1888. 7. Berlizheimer, “ Ueber einen Fall von Magentetanie,” “Berl. klin. Woch- enschr.,” 1897, xxxiv, 773-775. 8. Biernacki, “ Berl. klin. Wochenschr.,” 1891, Nr. 25 u. 26. 9. Boas, “ Ueber periodische Neurosen des Magens,” “ Deutsche med. Wochenschr.,” 1889. 10. Bourneville et Seglas, “ Du Merycisme,’ - “ Arch, de Neurologie,” Paris, 1883. 11. Bouveret, L., “ Traite des Maladies de l’Estomac,” Paris, 1893, p. 654. LITERATURE ON GASTRIC NEUROSES. 787 12. Bouveret et Devic, “ Recherches Cliniques et Experimentales sur la Tetanie d'Origine Gastrique,” “ Revue de M< 5 d.,” 1892, xn. 13. Brieger, “ Deutsche med. Wochenschr.,” 1880, Nr. 14. 14. Briigelmann, W., “ Ueber Hemicrania gastrica,” “ Berl. klin. Wochen- schr.,” 1883. 15. Buch, “ Wirbelweh eine neue Form der Gastralgie,” “ Petersb. med. Wochenschr.,” 1889. 16. Burkart, “ Zur Pathologie der Neurasthenia gastrica,” Bonn, 1892. 17. Cahn, “ Deutsches Archiv f. klin. Med.,” 1884, S. 402. 18. Cantarono, G., “ Neurolog. Centralbl.,” Bd. iv, 1885. 19. Cartier, “Action de la Feinture de Sode Centre le Vomissement,” “ L’Union Med.,” 1889. 20. Chantemesse et Le Noir, “ Nevralgies Bilaterales et Dilatation de l’Es- tomac,” “ Arch. G6n. de Med.,” 1885. 21. Charcot, “ Des Crises Gastriques Tabetique avec Vomissements Noirs,” “ Gaz. Med. de Paris,” Sept., 1892. 22. Charcot, “ Letjons sur les Maladies du Systeme Nerveux,” 1886. 23. Claus, “ Hysterisch onbedwing baar braken hyprotherapie,” “ Medisch. Weekblad,” 1896, 30, v. 24. Cordes, “ Die Platzangst, — Symptom einer Erschopfungsneurose,” “ Arch. f. Psych.,” Bd. ill, 1872. 25. Cordes, “ Einiges iiber Platzangst,” “ Archiv f. Psych.,” Bd. x, 1880. 26. Debove, “ Crises Gastriques non Fabetiques,” “ Bull, de la Soc. Med. des Hop.,” 1889. 27. Dehio, “ Singultus als Reflexneurose,” “ Berl. klin. Wochenschr.,” 1889. 28. Delamarre, “ Des Crises Gastriques dans l’Ataxie Locomotrice,” “These de Paris,” 1866. 29. Demange, “ Revue de Medecine,” 1892. 30. De Sere, L., “ Du Relachement du Pylore,” “ Gaz. des Hop.,” 1864, No. 62. 31. Doyen, “ Les Spasmes du Pylore, ses Rapports avec l’Hyperstenie Gas- trique,” “ Med. mod.,” Paris, 1897, vm. 32. Dubois, “ Crises Gastriques dans l’Ataxie Locomotrice,” “ These de Paris,” 1888. 33. Ebstein, “ Deutsches Archiv f. klin. Med.,” Bd. xxvi, S. 295. 34. Edinger, “ Deutsches Archiv f. klin. Med.,” 1881. 35. Edlefsen, “Ueber Husten und Magenhusten,” “Deutsches Archiv f. klin. Med.,” Bd. xx. 36. Edwards, L. B., “Gastralgia: Its Forms, Recognition, and Treatment,” “ Practice,” Richmond, 1897, xi, 62-74. 37. Einhorn, Max, “A Case of Dysphagia with Dilation of the Esopha- gus,” “ Med. Record,” 1888. 38. Einhorn, “ Eine neue Methode der directen Magenelektrisation,” “ Berl. klin. Wochenschr.,” 1891. 39. Einhorn, “Weitere Erfahrung iiber die directe Elektrisation des Ma- gens,” “ Zeitschr. f. klin. Med.,” 1893. 40. Erb, “ Handbuch der Elektrotherapie,” 2. Aufl., Leipzig, 1886. 41. Erb, “ Ueber die wachsende Nervositat unserer Zeit,” Prorectoratsrede, Heidelberg, 1893. ;88 NEUROSES OF THE STOMACH. 42. Ewald, “ Neurasthenica dyspeptica,” “ Verhandlungen des Congresses fiir innere Medicin,” 1884. 43. Ewald, “ Enteroptose und Wanderniere,” “ Berl. klin. Wochenschr.,” 1890. 44. Ewald, “ Some Forms of Gastralgia,” “ Internat. Clin.,” Philadelphia, 1898, 11. 45. Fenwick, “ On Atrophy of the Stomach and on Nervous Affections of the Digestive Organs,” London, 1880. 46. Fenwick, “ Hyperacid Dyspepsia,” “ Med. Press and Circ.,” London, 1897, LXIV. 47. Fenwick, “ Paroxysmal Hyperacidity in Children Simulating Migraine,” “ London Lancet,” January 8, 1898. 48. Fenwick, “ Hyperesthesia of the Mucous Membranes of the Stomach,” “Med. Press and Circ.,” London, 1898, lxv, 327. 49. Fenwick, “ Ueber spasmodische Strictur der Cardiaoffnungdes Magens,” “Wien. med. Bl.,” 1898, XXI, 327-344. 50. Ferrari, E., “Ectasia e tetania gastrica,” “ Practico,” Firenzo, 1897-98, in. 51. Fleiner, “Ueber die Veranderungen des Nervensystems bei Addison- scher Krankheit,” “ Zeitschr. f. Nervenheilk.,” 1892. 52. Fleiner, “ Ueber die Behandlung einiger Reizerscheinungen und Blut- ungen des Magens,” “Verhandlungen des XII. Congresses f. innere Medicin,” Wiesbaden, 1893. 53. Fleiner, “ Erfahrungen fiber die Therapie der Magenkrankheiten,” “ Sammlung klin. Vortrage,” 1894, Nr. 103. 54. Fleiner, “ Ueber Neurosen gastrischen Ursprungs, mit besonderer Beriicksichtigung der Tetanie und ahnlicher Krampfanfalle,” “Archiv f. Ver- dauungskrankh.,” Bd. 1, 1895. 55. Flemming, “ Ueber Pracordialangst,” “Allgem. Zeitschr. f. Psychiatrie,” Bd. v, 1848. 56. Fothergill, cf. Krakauer, “ Der Chron. Morb. Brightii der atherom. Process und das Blut in ihren Wechselbeziehungen,” Berlin und Neuwied, 1892. 57. Frankl-Hochwart, V., “ Die Tetanie,” Berlin, 1889. 58. Freund, E., “ Ueber Intoxications erythyme,” “Wien. med. Wochen- schr.,” 1894. 59. Fiirbringer, “Ueber Magenschwache,” “ Deutsche med. Zeitung,” 1893. 60. Gans, Edg., “IX. Congress f. innere Medicin,” Wiesbaden, 1890. 61. Garrigues, “Des Dyspepsies Hypo et Hypersteniques,” These de Mont- pelier, 1896. 62. Gassner, “ Ueber die bei Dilat. ventric. vorkommenden tonischen Muskelkrampfe und epileptiformen Anfalle,” Inaug. -Dissert., Strassburg, 1868. 63. Geigel und Abend, “ Die Salzauresecretion bei Dyspepsia nervosa,” “ Virchow’s Archiv,” Bd. cxxx. 64. Gerhardt, D., “ Zur Lehre von der Achylia gastrica,” “Berl. klin. Wochenschr.,” 1898, xxxv, 765-768. 65. Glax, G., “ Ueber den Zusammenhang nervoser Storungen mit den Erkrankungen der Verdauungsorgane ” und “Ueber nervose Dyspepsie,” “ Sammlung klin. Vortrage,” 1882, Nr. 223. LITERATURE ON GASTRIC NEUROSES. 789 66. Godart-Danhieux, “ La gastralgie nerveuse,” “ La Policlinique,” I, II, 1896. 67. Goldschmidt, E., “ Ueber den Einfluss der Elektricitat auf den gesunden und kranken menschlichen Magen,” “ Deutsches Archiv f. klin. Med.,” 1895, Bd. lvi. 68. Gull, “ Lancet,” 1868. 69. Gumprecht, “ Magentetanie und Autointoxikation,” “ Centralbl. f. innere Med.,” Leipzig, 1897, xvm, 569-593. 70. Hadra, B. E., “Neurosis of the Stomach from a Surgical Standpoint,” “Texas Med. Jour.,” Austin, i897~’98, 3cm, 319-344. 71. Halipre, “ Un cas de Dyspepsie Nervomotrice,” “ Normandie Medicale,” 1, vii, 1896. 72. Halliday, A., “The Condition of the Gastric Secretion in Merycism,” “ Med. Record,” New York, 1897, lii. 73. Hamilton, H. J., “ Hyperchlorhydria,” “ Canad. Pract.,” Toronto, 1897, XXII. 74. Havel, “ Des Crises Gastriques dans l’Ataxie Locomotrice,” “These de Paris,” 1882. 75. Hayem, “ Bull. Medicale,” 1891, No. 87. 76. Hayem, “ Sur Un cas de Chloro-dyspepsie avec Neurasthenie,” “ Med. Mod.,” 20 Janvier, 1897. 77. Hayem, “ De l’Hyperchlorhydrie par Saturation Alcaline,” Soc. Med. du Hop., 15 Avril, 1898. 78. Hayem, “ Sur la Gastralgie,” “ Rev. Gen. de Clin, et de Therap.,” Paris, 1898, xii, 353-357. 79. Henoch, “ Ueber Asthma dyspepticum,” “ Berl. klin. Wochenschr.,” 1876, Nr. 18. 80. Herz, M., “ Fall von motorischer Magenneurose,” “ Wien. klin. Wochen- schr.,” 1897, x, S. 1041. 81. Hildebrandt, W., “Nervose Storungen im Gefolge von Magenkrank- heiten.” 82. Hoffmann, A., “ Ueber den Einfluss des galvanischen Stromes auf die Magensaftabscheidung,” “ Berl. klin. Wochenschr.,” 1890. 83. Hoffmann, J., “ Zur Lehre von der Tetanie,” “ Heidelberger Habilita- tionsschrift,” 1888. 84. Honigmann, G., “ Ueber die Neurosen des Magens,” “ Zeitschr. f. prakt. Aerzte,” 1897, iv, pp. 833-857. 85. Hubbard, W. A., “ Medical Record,” July 31, 1886, p. 122. 86. Huefler, “ Miinch. med. Wochenschr.,” 1889, Nr. 33* 87. Hunt, B., “ On Nervous Vomiting,” “Clin. Jour.,” London, 1898, xii, pp. 238-240. 88. Hyde, “ Twentieth Century Practice of Medicine,” vol. v, p. 170. 89. Immermann,“Verhandlungen des Congresses fur innere Medizin,” Wies- baden, 1889. 90. Jacobi, A. .“Transactions of the Association of American Physicians,” 1894. 91. Jacobson and Ewald, “Ueber Tetanie,” “Verhandlungen des Congresses fur innere Medizin,” 1893. 92. v. Jaksch, “ Epilepsia acetonica,” “ Zeitschr. f. klin. Med.,” Bd. x. 93. Johannessen, “ Zeitschr. f. klin Med.,” Bd. x, S. 274. 52 790 NEUROSES OF THE STOMACH. 94. Jones, Allen A., “Gastric Conditions in Renal Disease,” “ N. Y. Med. Jour.,” Jan. 19, 1895. 95. Joslin, E. P., “ Hyperacidity of the Stomach and its Treatmeat,” “ Bos- ton Med. and Surg. Jour.,” 1898, cxxxvm, pp. 389-392. 96. Jiirgensen, “ Ueber Abscheidung neuer Formen nervoser Magenkrank- heiten,” “ Deutsches Archiv f. klin. Med.,” Bd. xliii. 9 7. Jiirgensen, C., “ Ueber die Diat bei der Superaciditat : eine kritische Litteraturstudie,” “ Archiv f. Verdauungskrankh.,” Berlin, 1897,111. 98. Kahler, “ Prager Zeitschr. f. Heilkunde,” Bd. 11. 99. Kaufmann, J., “ Zwei Falle geheilter pernicioser Anamie, nebst Bemer- kungen zur Diagnose und Therapie dieser Krankheit,” “ Berl. klin. Wochen- schr.,” 1890, Nr. 10. 100. Klemperer, “ Berl. klin. Wochenschr.,” 1899, Nr. 11. 101. Koerner, “ Deutsches Archiv f. klin. Med.,” Bd. X, S. 274. 102. Koziczkowsky, E. von, “ Beitrag zur Aetiologie der Magenneurosen,” “ Berl. klin. Wochenschr.,” Nr. 7, 1897. 103. Kussmaul, “ Ueber die Behandlung der Magenerweiterung durch die Magenpumpe,” “ Deutsches Archiv f. klin. Med.,” 1869, Bd. VI. 104. Kussmaul, “ Die peristaltische Unruhe des Magens,” “ Sammlung klin. Vortrage,” 1880, Nr. 18 1. 105. Kutneff, “ Neurasthenie, Herabsinken von Bauchorganen und gastro- intestinale Atonie,” Ref. in the “ Jahresberichte,” 1894, Bd. 11. 106. Laffitte, “ Des Crises Gastriques,” “ Gaz. des Hop.,” Jan., 1894. 107. Landouzy et Dejerine, Societe de Biologie, 1884. 108. Leo, “ Ueber Bulimie,” “ Deutsche med. Wochenschr.,” 1889, Nr. 29 u. 30 - 109. Leube, “Ueber nervose Dyspepsie,” “ Deutsches Archiv f. klin Med.,” 1878, Bd. xxiii. no. Leven, “ Estomac et Cerveau,” Paris, 1884. in. Leven, “ Phenomenes Nerveux lies a la Dyspepsie,” “ Gaz. des Hop.,” 1880, No. 40. 1 12. Leven, “ Phenomenes Nerveux qui se Produisent sous l’lnfluence de la Dyspepsie,” ibid., 1880, No. 137. 1 13. Leyden, “Ueber Anfalle von periodischem Erbrechen, nebst Bemerk- ungen fiber nervose Magenaffectionen,” “ Zeitschr. f. klin. Med.,” Bd. iv, 1882. 1 14. Liebmann, G., “ Meine Erfahrungen mit Hyperaciditat,” “New Yorker med. Monatsschr.,” 1897, IX, 311-318. 1 1 5. Liell, E. W., “The Relation of the Pregnant Uterus to the Reflex Nausea and Vomiting Accompanying Gestation,” “ Amer. Medico-Surg. Bull.,” 2i, xi, 1897. 1 16. Littig, L. W., “Gastric Neuroses,” Transactions Iowa Medical Society, Burlington, 1898. 1 17. Loeb, M., “ Tetanie bei Magenerweiterung,” “Deutsches Archiv f. klin. Med.,” 1890, Bd. lxvi. 1 18. Luzzato, A. M., “ Un caso di mericissmo connotevoli alterazioni del chimismo gastrico,” “ Riv. Ven. di Scienze Med.,” hi, p. 116. 1 19. Lyman, H. M., “Nervous Dyspepsia,” “Jour. Amer. Med. Assoc.,” 1897, xxviii, pp. 959-962. LITERATURE ON GASTRIC NEUROSES. 79 1 120. Malbranc, “ Ueber Behandlung von Gastralgieen mit der inneren Magendusche,” etc., “ Berl. klin. Wochenschr.,” 1878. 121. Marcus, A., “ Ein Fall von hysterischer Magenneurose (unstillbares Erbrechen) compliciert mit Diabetes insipidus bei einem Manne,” Dissert., Miinchen, 1896-97. 122. Mariani, “ De 1 ’ Hypersecretion Gastrique,” Th&se de Montpellier, 1896. 123. Mathieu et Milan, “Etude sur le Pituite Hemorragique des Hyster- iques,” Paris, 1896. 124. Maybaum, J., “ Archiv f. Verdauungskrankh.,” Bd. 1, Heft 4. 125. Melzer, S. J., “Berl. klin. Wochenschr.,” 1888, Nr. 8. 126. Mitchell, Weir, “ Fat and Blood,” Philadelphia, 1884. 127. Mobius, S. A., “ Ueber die schmerzstillende Wirkung der Elektricitat,” “ Berl. klin. Wochenschr.,” 1880. 128. Mongour et Lafarelle, “ Spasme du Pylore,” “Jour, de Med. de Bor- deaux,” 1898, xxviii, p. 176. 129. Muller, Fr., “ Tetanie bei Dilatatio ventriculi und Achsendrehung des Magens,” “ Charite Annalen,” 1888, Bd. xm. 130. Murdoch, F. H., “The Absence of Hydrochloric Acid in the Stomach, with Report of Cases,” “ Phila. Med. Jour.,” 1898, 1. 1 3 1 . Murdoch, F. H., “ Nervous Dyspepsia, with Report of Cases,” “ N. Y. Med. Jour.,” 1898, lxviii, pp. 437-439. 132. Muret, “Hyperemesis gravidar. und Hysterie,” “Deutsche med. Wochenschr.,” 1893. 133. Naunyn, “ Zur Lehre vom Husten,” “ Deutsches Archiv f. klin. Med.,” XXIII. 134. Neumann, “ Deutsche Klinik,” 1861, Nr. 3. 135. Nonne, “ Beitrage zur Kenntniss der im Verlaufe der perniciosen An- amie beobachteten Spinalerkrankungen,” “Archiv f. Psychiatrie,” Sep. H., Bd. xxv. 136. v. Noorden, “ Klinische Untersuchungen iiber die Magenverdauung bei Geisteskrankheiten,” “Archiv f. Psychiatrie und Nervenkrankheiten,” Bd. x. 137. v. Noorden, “ Pathologie der gastrischen Crisen,” “Charite Annalen,” 1890. 138. Oettinger, W., “Idiopathic Gastric Crises; Periodical Vomiting of von Leyden,” “ Med. Weekly,” 1897, v, pp. 374-376. 139. Olivetti, B., ed. Muggia, A., “ Azione della pilocarpina sulla secrezione chlorata del ventricolo nell ipoedana-chloridria,” “ Gazz. med. di Torino” 1897, xlviii, 661-666. 140. Olivetti, B., “ Fleiner’s Methode in der Behandlung der Hyperchlor- hydrie,” “ Therapeutische Monatshefte,” Berlin, 1898, xn. 141. Oppenheim, “Berl. klin. Wochenschr.,” 1885. 142. Oser, “Die Neurosen des Magens und ihre Behandlung,” “Wiener Klinik,” 1885, Heft 5 u. 6. 143. Pacanowski, “ Deutsches Archiv f. klin. Med.,” Bd. XL. 144. Panecki, “ Retroflexio uteri und Magenneurose,” “ Therapeutische Monatshefte,” 1892. 145. Petitjean, “ Contribution a l’litude des Crises Gastriques dans l’Ataxie Locomotrice,” “These de Paris,” 1874. 792 NEUROSES OF THE STOMACH. 146. Pettyjohn, E. S., “ Functional Gastric Diseases and their Treatment,” “ Physician and Surgeon,” Detroit and Ann Arbor, 1897, xix, pp. 258-262. 147. Peyer, A., “ Beitrag zur Kenntniss der Neurosen des Magens und des Darms,” “ Correspondenzblatt f. Schweizer Aerzte,” 1888. 148. Pick, A., “ Ueber Hyperasthesie des Magens,” “ Wiener med. Wochen- schr.” 1898, xlviii. 149. Pidoux, “Rapport de l’Herpetisme et des Dyspepsies,” “ L’Union Med.,” 1866, p. 235. 150. Ponsgen, “Die motorischen Verrichtungen des menschlichen Magens,” Strassburg, 1882, S. 127. 1 51. Potain, “ Paralysie Consecutive a des Troubles Digestifs,” “ Gaz. des Hop.,” 1880. 152. Raymond, “Des Dyspepsies,” “These d’aggreg.,” 1878. 153. Reed, B., “The Excessive Secretion of Hydrochloric Acid by the Stomach, and its Possible Serious Consequences,” “ Internat. Clin.,” 1897. 154. Reed, B., “ A New Intragastric Electrode for the Treatment of Gas- tralgia and Deficient Gastric Motility with or without Dilation,” “ Phila. Med. Jour.,” 1898, 1. 155. Remond (de Metz), “ Des Crises Gastriques Essentielles,” “ Arch. Gen. de Med.,” 1889, Tome 11. 156. Renvers, “ Berl. klin. Wochenschr.,” 1888, No. 53. 157. Richet, Ch., “Du Sue. Gastrique chez 1 ’Homme et les Animaux,” Paris, 1878. 158. Richter, “ Ueber nervose Dyspepsie und nervose Enteropathie,” “Berl. klin. Wochenschr.,” 1882. 159. Riegel, F., “ Zur Lehre von der Tetanie,” “Deutsches Archiv f. klin. Med.,” 1873, Bd. Xil. 160. Riesmann, D., “ Stomach from a Case of Rumination,” “ Tr. Path. Soc.,” Philadelphia, 1898, xviii, p. 120. 161. Robin, A., “ Gastro-succhoree et Stenose Pylorique,” “ Courier med.,” Paris, 1897, XLVii, p. 169. 162. Rockwell, A. D., “Atonic or Nervous Dyspepsia and its Treatment by Intragastric Electrization,” “ Internat. Clin.,” 1898. 163. Rosenberg, O., “Beitrag zur Lehre von den Krankheiten des Verdau- ungsapparates,” “ Deutsche med. Wochenschr.,” 1879 (Vagusneurose). 164. Rosenbach, O., “Die Emotionsdyspepsie,” “Berl. klin. Wochen- schr.,” 1897. 165. Rosenheim, Th., “ Berl. klin. Wochenschr.,” 1890. 166. Rosenheim, Th., “Ueber nervose Dyspepsie,” “Berl. klin. Wochen- schr.,” 1897, Nr. 34. 167. Rosenstein, “ Berl. klin. Wochenschr.,” 1890, No. 13. 168. Rosenthal, “ Magenneurosen und Magenkatarrh,” Wien und Leipzig, 1886. 169. Rossbach, “ Nervose Gastroxynsis als eine eigene characterisirbare Form der nervosen Dyspepsie,” “ Deutsches Archiv f. klin. Med.,” Bd. xxiv. 170. Sansom, A. E., “ A Note on Neuropathic Dyspepsia and its Correlations with Disturbances of the Rhythm of the Heart,” “Lancet,” London, 1897, 11. 17 1 . Sansom, L., “Sulla pathogenesi dell iperchloridria primitiva,” “Ref- orma med. Napoli,” 1897, xm. LITERATURE ON GASTRIC NEUROSES. 793 172. Schetty, F., “ Deutsches Archiv f. klin. Med.,” lid. xliv, S. 219. 173. Schnitzler, J., “ Ueber einen Krampftumor des Magens, nebst Bemerk- ungen zum sog. Spasmus pylori,” “ Wiener med. Wochenschr.,” 1898, xlviii. 174. Schuchardt, “ Epileptiforme Anfalle bei Magenerkrankungen,” “ All- gem. Zeitschr. f. Psychiatrie,” 1882, Bd. xxxvm. 175. Schiile, A., “ Einige Bemerkungen iiber die Hyperaciditat ; die Diat bei derselben,” “Archiv f. Verdauungskrankh.,” 1897, Heft in. 176. Schiitz, “ Prager med. Wochenschr.,” 1882, Nr. II. 177. See, G., “ Anwendung der Cannabis indica in der Behandlung der Neurosen und gastrischen Dyspepsien,” “ Deutsche med. Wochenschr.,” 1890. 178. Singer, “ Die Rumination beim Menschen und ihre Beziehung zum Brechact,” “ Deutsches Archiv f. klin. Med.,” 1893, Bd. Li. 179. Sinkler, W., “ Rumination in Man,” “Jour. Amer. Med. Assoc.,” April 9, 1898. 180. Smith, D. E., “ Hyperchlorhydria,” “ Northwest Lancet,” St. Paul, XVII. 181. v. Sohlern, “ Zur Behandlung der nervosen Magenkrankheiten,” “ Berl. klin. Wochenschr.,” 1891. 182. Sollier, “ Revue de Medecine,” Aout, 1891. 183. Somers, L. S., “ Merycism,” “Medical Record,” 17, iv, 1897. 184. Sorens, O., und Metzger, L., “Ueber die Diat bei Superaciditat,” “ Miinch. med. Wochenschr.,” 1898, xlv. 185. Stiller, “ Die nervosen Magenkrankheiten,” Stuttgart, 1884. 186. Stockton, “ Medical Record,” 1894. 187. Strauss, “ Des £cchymoses Fabetiques a la Suite des Crises Doulour- euses,” “Arch, de Neur.,” i88o-’8i. 188. Strauss, “ Ueber das Vorkommen von Ammoniak im Mageninhalt,” etc., “ Berl. klin. Wochenschr.,” 1893. 189. Talma, “ Zur Kenntniss des Leidens der Bauchsympathicus,” “ Deutsches Archiv f. klin. Med.,” 1892, Bd. xlix ; “ Zeitschr. f. klin. Med.,” 1884, Bd. viii, S. 407. 190. Tere, “ Note pour Servis a l’Histoire des Troubles Gastrique de l’Epi- lepsie et de l’Heredite Morbide Progressive,” “Journal de Neurologie,” 5, in, 1896. 191. Tournier, C., “ Ouelques cas de Vomissements Nevrosques,” “ Province Med.,” Lyon, 1897, xi. 192. Trousseau, “ Med. Klinik des Hotel Dieu” in Paris, Bd. in, 1868, Cap. 67. 193. Upshur, J. N., “ Gastralgia, with Report of a Case,” “Medical Reg- ister,” Richmond, 1897, 1, 31. 194. Wagner, G., “ Zur Behandlung der Superaciditat des Magens mit Bergmann’schen Magenkautabletten,” “ Therap. Monatshefte,” Berlin, 1897, XI. 195. Westfallen, “ Kopfschmerzen gastrischen Ursprungs,” “ Berl. klin. Wochenschr.,” 1891. 196. Westphal, C., “ Ueber Agarophobie, eine neuropathische Erscheinung,” “ Archiv f. Psychiatrie,” 1872, Bd. ill. 197. Whitney, H. B., “ Cyclic Vomiting: A Brief Review of this Affection as Illustrated by a Typical Case,” “ Arch. Pediat.,” 1898, xv. 794 SENSORY NEUROSES. 198. Hemmeter, J. C., “ Experimental Basis of the Treatment of Hyper- acidity,” etc., “ Journ. Am. Med. Assoc.,” Oct. 9, 1897. 199. Hemmeter, J. C., “ Histologie d. Magendriisen bei Hyperaciditat,” “Archiv f. Verdauungskrankh.,” Bd. iv, 98, S. 23. CHAPTER XI. SENSORY NEUROSES. HYPERESTHESIA. Hyperesthesia depends upon a morbid increase in the irritability of the sensory nerves of the stomach. It is probably a neurosis of the vagus, and a mild form of gastralgia. Clinically, the two forms of gastric sensibility — viz., gastralgia and hyperesthesia — are differentiated by the following facts : The unpleasant sensation of pressure, fullness, and pain in the epigastrium, with eructations, nausea, and vomiting, occur in hyperesthesia only after the inges- tion of food : that is, there must be a digestive stimulation of the mucosa. The distress occurs only after meals, very rarely with an empty stomach ; but in gastralgia the pains and other distress occur with equal intensity in the full as well as in the empty stomach ; digestive irritation is not necessary to cause gastralgia. Hyperesthesia lasts several days, weeks, or even months, with uniform or gradually increasing intensity, and during this time dyspeptic symptoms occur daily after every meal ; in gastralgia, however, the pains last during the attacks, generally for a few hours only. In the intervals between the attacks the excitability of the nerves is so completely arrested that even strong irritation — like the overloading of the stomach with food — does not cause a return of the pain. The various acts constituting normal diges- tion, the movements of the gastric wall and of the contents of the digestive tract, are phenomena of which a healthy person is not conscious, but they may be perceived by patients with increased sensitiveness of the gastric nerve-endings. As a result of this nervous state sensations reach consciousness from these localities which in the normal being would not pass the threshold of con- sciousness. The disturbance of the nerves need not necessarily be in the end distributions of the stomach ; they may be in the nerve itself GASTRIC HYPERESTHESIA. 795 or in the central organ. Most frequently the seat may be in the per- ipheral nervous end organs in the stomach ; these are the cases that have been caused by improper mode of life and various insults to the mucosa. In other rare cases the gastric hyperesthesia may be a perception due to increased excitability of the nervous centers. In order to intelligently appreciate the sufferings of patients with increased sensibility it is necessary to bear in mind that the increased irritability brings about the perception of transactions into the digestive tract which in themselves are not pathological, and if present to the same degree in a healthy individual, would not be perceived. The natural process of digestion and absorption in such patients is a train of uninterrupted distressing sensations. The patients themselves generally misinterpret their condition or exaggerate it, and as a consequence of the various impressions that they perceive, assume that they suffer from severe organic disease. They often become hypochondriacal. Hyperesthesia may be an independent, idiopathic or secondary, symptomatic neurosis. Causation. — The primary idiopathic form occurs very frequently as an accompaniment to chlorosis and anemia, particularly with women and young girls. Also after repeated overloading of the stomach with indigestible food. Long-continued use of very salty or acid or spiced foods, and the ingestion of very hot or very cold drinks after long fasting, and in debilitated states following excesses in Venere et Baccho. It has been observed to occur also after chloroform narcosis. Secondary hyperesthesia occurs with hy- peracidity and supersecretion in hysterical patients, also in neu- rasthenia and tabes. Gastralgia may follow hyperesthesia, and there are cases in which both neuroses may exist simultaneously. Symptomatology. — Patients with this neurosis frequently feel the pulsations of the abdominal aorta, and complain of beating and pulsating in the stomach. Then, again, they have a feeling of heat or cold, or a gnawing, burning sensation, and an impression of rest- lessness through the entire stomach. The ingestion of food, no matter of what consistency, causes a sensation of discomfort, full- ness, nausea, and even vomiting. These sensations may increase to a typical gastralgia, and are felt only during the first period of digestion, or they may last as long as food is contained in the stomach. Some patients complain for a while even after food has left the stomach. The pains are absent in the morning, when the stomach is entirely empty. If the hyperesthesia depend upon 79 6 SENSORY NEUROSES. hyperchylia, the pains do not become pronounced until the second period of gastric digestion, when the acidity of the gastric chyme reaches its highest degree. In some cases of hyperesthesia it may happen that the distress is temporarily relieved by the ingestion of albuminous food or the taking of alkalies. The burning, sticking, and beating in the stomach may be accompanied by bulimia. These gastric symptoms are generally accompanied by other ner- vous phenomena which are probably symptoms of the fundamental etiological disease ; thus we meet with migraine, cephalalgia, and neuralgia in other parts of the body, etc. The emesis which occurs in hyperesthesia induces the patients to restrict their diet more and more, whereby the general nutrition and bodily resist- ance become very much reduced. Concerning the appetite and the foods which are best digested, the patients show the most manifold contrasts. Some of them feel more distress after liquids than after solids. The appetite does not seem much affected ; some patients have an intense feeling of hunger. There are no very constant anomalies of motility or secretion. The bowels are generally constipated. Prognosis. — The prognosis is favorable, as the hyperesthesia ceases when the detrimental and irritating conditions which excite the sensibility of the stomach can be kept away, and when the fundamental disease can be removed. Diagnosis. — The affection may be confounded with gastralgia, and with the painful symptoms of organic gastric diseases. From gastralgia it can be distinguished by the fact that the symptoms occur daily for a long time, regularly after each meal, and that they are absent when the stomach is empty. Gastralgia occurs only spasmodically, rarely lasts longer than several hours, and is of equal severity in an empty as in a full stomach. The intervals between the attacks are perfectly free from gastric distress. Concerning the differential diagnosis between hyperesthesia and the distress of diseases of the stomach connected with anatomical alterations, we refer to the differential points stated in the diagnosis of gastralgia. We might emphasize here that, in the organic dis- eases, the pains are entirely absent when the stomach is empty. Atrophic gastritis forms an exception to this rule. The intensity of the pains is influenced by the quality of the food, which is not the case in hyperesthesia, and that organic diseases are mostly associated with tolerably constant disturbances of secretion and motility. GASTRIC IDIOSYNCRASIES. 797 Treatment. — The treatment will be directed in the first place to the correction of the underlying fundamental disease. Wherever this is not possible, or wherever an idiopathic form of hyperesthesia is present, all irritants which can exert detrimental influence upon the stomach must be excluded. All bodily and mental exertion must be avoided. In severe cases the Weir Mitchell rest-cure, to- gether with a Leube ulcer cure, has, in our experience, been very efficacious. Hot, moist applications to the stomach are very sooth- ing. In a very pronounced case of gastric hyperesthesia in a col- league, which returned regularly whenever he was under great mental strain, the symptoms disappeared entirely after a sojourn at the seashore for one month. Galvanization is a capital method of treating this affection. The intragastric method may be used, but when the patient is not accustomed to the swallowing of the elec- trode, we have obtained good results from the external application of the large abdominal plates. Use of tea, coffee, tobacco, and alcohol must be avoided, as these things have been known to keep up a hyperesthesia. Rosenheim has suggested the following treat- ment (“ Berlin, klin. Wochenschr.,” 1890) internally : R. Argenti nitras, 0.2 gr. iij Aquae menthse pip., 100.0 ^ iij. M. SlG. — Two teaspoonfuls in a wineglassful of water, on an empty stomach, in the morning, and a half-hour before each meal. The patient must be kept in bed, and warm cataplasms applied to the epigastrium. The diet consists of milk taken by table- spoonful doses, later on soft eggs, and scraped beef and dipped toast. When the stomach becomes more resistant, the patient may return to solid food. To remove the cause, Rosenheim advises treat- ment of the general underlying affection, bodily and mental rest, and hydrotherapeutic measures. Severe hyperesthesia is some- times relieved by bromid of strontium and codein. We have also obtained very good results from spraying the stomach with a solu- tion of morphin, cocain, and menthol. In doing this, a spray must be used by which we can tell the exact amount of cocain and morphin which reaches the stomach with the spraying liquid. It is well not to put more into the spray than we wish to put into the stomach, otherwise the patient may absorb too much cocain and morphin. Gastric idiosyncrasies are those peculiar forms of hyperesthe- sia in which neuropathic and sometimes perfectly healthy persons 79B SENSORY NEUROSES. have morbid sensations only after ingesting certain foods. These sensations consist of headache, light fever, skin erythema, and urticaria. The author has observed persons who developed urti- caria after eating crabs, potatoes, cheese, or strawberries. One of our patients regularly develops an acute acne whenever she eats cheese. Another patient regularly develops fever, eructations, nausea, and vomiting whenever he partakes of crabs. Although a heightened irritability of the sensory nerves may be instrumental in the devel- opment of these idiosyncrasies, it is very plausible that autointox- ication plays a very important role in them. It is probable that in individuals who develop urticaria after eating certain foods, there must be microorganisms that develop toxins from these foods which, in turn, act in the manner indicated. Pick states that his cases suffered also from constipation, which naturally favors the putrefaction of the ingesta. Acting upon the theory of autointox- ication caused by intestinal putrefaction, Pick very strongly recom- mends the internal use of creasote (see “Albu. Autointoxica- tionen des Intestinaltractus,” part on The Skin, p. 88 ; also p. 396 of this volume), which in my experience has proved useless. The correct course to follow is to avoid all foods entirely that are known to cause such distress. GASTRALGIA (Cardialgia ; Gastrodynia). Gastralgia, or neuralgia of the stomach, occurs in periodical and spasmodical attacks of severe gastric pain, alternating with inter- vals of freedom from pain. Pains of greater or less intensity occur with all gastric diseases, particularly with ulcer, carcinoma, gas- tritis atrophicans, and toxic gastritis. These pains are a consequence of the anatomical alterations which these organic diseases effect in the gastric wall, brought about most probably by exposure, dis- tortion, and compression or inflammation of the sensory gastric nerves. Such pains have been described in the chapter on various Organic Diseases of the Stomach. Gastralgic pain results from func- tional, not from structural, disturbances of the sensory nerves. Gas- tralgia is characterized by the irregular intervals in which it occurs, and its independence of the quality and quantity of the ingesta. The attacks come on either suddenly, or there may be such pre- monitory symptoms as feeling of pressure and fullness in the stom- ach, eructation, nausea, vomiting, headache, and salivation. The pains have a gnawing, boring, burning, tearing, or cramp-like char- acter. They are felt principally in the epigastric region. In some GASTKALGI A. 799 cases the pain radiates to the hypochondriac regions, the entire abdomen and back, and may be accompanied by unmistakable signs of collapse and the feeling of impending dissolution. The pains occur as well after food that is easily digestible as after indi- gestible food. In some hysterical patients the so-called “ clavus hystericus,” a sharply localized pain, as if a nail were driven into apart, is well described by the sufferer. There is also, in some of these cases, a sudden and transient sensation as if a tremendous ball were rising in the throat (globus hystericus). Nausea and vomiting, as well as bulimia and an urgent desire to urinate, are occasional symptoms. The paroxysms may last a few minutes or several hours, and extend through the entire night; they may begin at any hour of the day or night. The intervals of relief may amount to days, weeks, or months. Malaria . — We have observed a number of cases of malarial gas- tralgia in which the attacks occurred at regular intervals, and could be distinctly associated with an evolution of the characteristic malarial parasite in the blood. These malarial gastralgias are not infrequent in fishermen, and even in sportsmen who sojourn for weeks along the shores of the Chesapeake Bay in Maryland. In a patient of this city the gastralgic attacks persisted, notwithstanding the most careful treatment, until the patient could be persuaded to give up his ducking sport on the Chesapeake Bay, for the relief afforded by quinin was not permanent. The attacks occur gener- ally without any demonstrable cause. As a rule, only one attack occurs in the day, but there may be as many as four in one day. The end of the attack may culminate in very profuse vomiting, which brings a great relief, the pains ceasing thereafter as rapidly and suddenly as they came on. Gastralgia maybe a primary idio- pathic and independent disease or a secondary reflex neurosis. Causation. — The gastralgia is frequently a result of motor or secretory neuroses — of gastrospasm, pylorospasm, and cardio- spasm, hyperacidity, and supersecretion. The root of the vagus nerve maybe irritated by functional and anatomical diseases of the medulla and adjacent portions of the central nervous system. Boas (/. c., ii, S. 214) enumerates the following causes of gastral- gia : (1) Those that attack the stomach itself and its immediate surroundings. (2) Central causes. (3) Infections and intoxications. (4) Reflex causes emanating from other organs. (5) Neurasthenia and hysteria, (a) The causes that emanate from the stomach and 8oo SENSORY NEUROSES. its immediate surroundings are gastric ulcer, gastric carcinoma, gas- tritis acida and atrophicans, various forms of perigastritis, and peri- tonitic adhesion with the pancreas, liver, gall-bladder, spleen, and transverse colon, and other portions of the intestines. Furthermore, hypersecretion andgastroxynsis, tumors of neighboring organs, and pancreatic cysts. ( b ) Of the central causes, he mentions the attacks occurring with tabes (“ crises gastriques ”). In myelitis and brain tumors, gastralgic pains have been observed. ( c ) Infections and intoxicants may cause gastralgia. Of the first, a prominent cause of infection in our latitude is malaria, either in its outspoken form or in its masked and latent type. Of intoxicants, nicotin poisoning and the autointoxication associated with uric acid and gout are well-known causative factors. ( d ) Among the reflex causes emanating from other organs, diseases of the genito-urinary organs occupy the first place in both sexes. Prominent among these are displacements of the uterus, inflammations of the ovaries and tubes, and uterine and ovarian neoplasms. (Panecki,“ Retro- flexio uteri und Magenneurosis,” “ Therapeut. Monatsheft,” 1892, S. 79.) Independent organic gastric diseases that occur simultane- ously must be carefully differentiated from the typical gastralgia. Gastralgias may be associated with genito-urinary diseases in the male. (Peyer, “ Ueber Magenaffectionen b. mannlichen Genitallei- den,” “ Volkmann’s Samml. klin. Vortr.,” No. 356.) The gastralgias that occur as a consequence of enteroptosis have been fully con- sidered in the chapter on Gastroptosis. ( e ) Stomach neuralgia which occurs in hysterical and neurasthenic persons without any apparent cause, and those which occur in anemic patients, should prompt a very careful examination before we decide that there is no real organic trouble at the foundation of the gastralgia. Occasionally we may find that gastralgias occur with small median herniae of the linea alba. Whenever motor insufficiency exists with these herniae, we presume that the omentum is fixed in the hernial sac. Such cases have been recently reported by Charles D. Aaron and Rosen- heim (“ Berlin, klin. Wochenschr.,” 1897, No. 1 1). Horner (“ Ueber Cardialgia, Verursacht d. praeperitoneale Lipome,” “ Prag. med. Wochenschr.,” 1892, S. 310) reports a case of severe gastralgia caused by preperitoneal lipomata. These herniae of the linea alba can be treated successfully only by an operative or orthopedic method (bandages). F. Bardenhauer (“ Ueber den epigastrischen medianen Bauch- bruch,” in “ Gesammelte Beitrage a. d. Gebiete d. Chir. u. Medi- GASTRALGl A. 801 ' zin,” etc., Wiesbaden, 1893, S. 35), Vulpius (“ Beitr. z. klin. Chirurg.,” Bd. vii, H. 1), and Roth (“ Archiv f. klin. Chirurg.,” Bd. xlii, H. 1, S. 1) consider this subject from the surgical side. It is possible that in some cases of gastralgia in which we can not find other diseased conditions that may have caused the affections, second- ary anatomical changes in the stomach may exist. Among these are erosions without hemorrhage, follicular inflammation, adhe- sions with neighboring organs, and cicatrices.* These conditions can not be excluded with certainty, because they may not cause symptoms for a long time. Every caution should be exercised in the diagnosis of idiopathic gastralgia, as many a case that is diag- nosed as a genuine form of gastralgia of this character is found, after a very thorough examination, to be a result of some ana- tomical change, or a motor or secretory neurosis of the stomach, or of a disease of some other organ. Idiopathic gastralgia should be diagnosed only when symptoms and indications of other dis- eases can not be discovered after an exhaustive anamnesis, and repeated thorough examinations, and instituted during the intervals between the attacks when the patient is free from suffering. The author has rarely made the diagnosis of idiopathic gastralgia. Idiopathic gastralgia may occur in connection with chlorosis, anemia, chronic nicotin poisoning, nephritis, incipient tuberculosis, and convalescence from continued fevers, and also as a result of alcoholic and sexual excesses. The gastralgias which occur with arthritis, malaria, and chronic rheumatism are particularly inter- esting from an etiological point of view. We have repeatedly observed that gastralgic attacks in gout may take the place of an expected acute attack of the joints. The association of malaria with gastralgia can be established beyond a doubt by the blood examination for the malarial parasite, and this kind of gastralgia can be cured by the administration of quinin and sometimes of arsenic, and ceases entirely if the patient removes to an environ- ment that is free from malaria. The occurrence of gastralgia during gout has been explained by some by assuming that the deposits of uric acid and uric acid salts actually occur in the walls of the stomach and thereby irritate the endings of the sensory * A negro suffering from the most intense gastralgia with hyperacidity was operated on at the Maryland General Hospital by Dr. John D. Blake, upon the author’s advice. The stomach was bound to the liver, diaphragm, and transverse colon by numerous adhe- sions, those going to the liver being inseparable. 802 SENSORY NEUROSES. nerves. This theory explains how gastralgia may occur vicariously in place of expected attacks of gout. Secondary Gastralgia. — Cases of this type have been reported which were very severe and obstinate during life, and in which tumors were found at the autopsy drawing upon or compressing the fibers of the vagus and sympathetic. It has been observed, also, in Basedow’s disease, but is more frequently the result of direct or indi- rect irritation of the roots of the vagus nerve in consequence of organic or functional disease of the spinal cord or brain. We have already referred to the frequent attacks of gastralgia occurring in tabes, which have recently been explained by a sclerotic degenera- tion of the nucleus and of the main stem of the vagus (Kahler, Oppenheim, Demange, Dejerine). The gastric crisis, which we have described elsewhere, demands a greater interest because it may occur in tabes as an initial symptom when the other char- acteristic signs, such as absence of the tendon reflexes, rigidity of the pupils, and Romberg’s symptom, are not yet present, and in some cases the typical ataxia has not been known to occur for from six months to a year after critical gastralgias of this kind. Erb has established a very probable causal relation between syphilis and tabes, and the hope has been expressed that these early gastric crises should stimulate exhaustive clinical examinations of the patients with a view to combating the disease by mercury and iodids at a time when the spinal changes are not far progressed. Leyden has described gastralgia with subacute myelitis, and Oser with myelitis due to compression. Symptomatology. — The symptoms of the attacks are generally quite characteristic, and the course so typical that they can not be misinterpreted. Prodromal symptoms, such as depressed spirits, headache, salivation, nausea, pressure, and fullness in the stomach may occur, but, as a rule, are not observed and have no diagnostic value. Generally, the cases begin very suddenly with severe gas- tric pains, which are sometimes so intense as to baffle description. Strong pressure upon the stomach sometimes relieves the pain — in fact, the patients are often found doubled up in bed, pressing both hands upon the epigastrium. If the pain has been caused by hyperchylia, it is relieved by alkalies or albuminous food. The bowels are constipated and the urine is suppressed. The forehead is covered with large drops of cold perspiration, the pulse is small, occasionally irregular and accelerated. In rare cases it has been reported to have been much retarded. Great prostration and DIAGNOSIS OF GASTRALGIA. 803 muscular cramps, and even general convulsions, have been known to follow. At the end of the attack the patients usually indulge in repeated yawning, eructation, and sometimes vomit- ing, and in hysterical patients a copious dilute urine is sometimes voided. Diagnosis. — As idiopathic gastralgia can rarely be logically diagnosed, it will be more correct to consider gastralgia as a symp- tom, not as a disease perse; although the fundamental disease causing it may remain obscure or be missed entirely in the begin- ning of the disease, it may become pronounced eventually. Gas- tralgias may have to be differentiated from the pain of ulcer, acute and chronic gastritis, toxic gastritis, carcinoma, from rheumatism of the abdominal muscles, myalgia, intercostal neuralgia, nephrolithi- asis, cholelithiasis, and intestinal colic. The differential diagnosis from ulcer of the stomach has been stated in the chapter on Ulcer. The ulcer pain is sharply circumscribed in the epigastrium and in the dorsal regions. It is directly dependent upon the quantity and quality of the food. Pains from gastric ulcer are relieved by rest in bed, and made worse by movement. This pain does not occur in paroxysms — it is usually a lasting discomfort. There may be atypical cases of ulcer in which the diagnosis becomes much involved. Boas (/. c. y S. 38) emphasizes the diagnostic value of the painful point situated at the left of the spinal column between the tenth and twelfth thoracic vertebrae in cases of gastric ulcer. Von Leube advises, when other symptoms are missing, to treat the disease as if it were ulcer, and Boas recommends the internal administration of nitrate of silver for three or four weeks. The good result of both of these treatments would speak for gastric ulcer. The acute and chronic gastritis are rarely so painful as to be confounded with gastralgia. The pains of chronic atrophic gastritis occur only at a time when complete atrophy of the mucosa has supervened; and, inasmuch as the secretion in gastralgia is, as a rule, not suppressed or lost, this factor will constitute an important diagnostic feature, since HC 1 is, in a great majority of cases, absent in gastritis. From toxic gastritis the diagnosis is made by help of the clinical history; from carcinoma, by means of ascertaining the state of the motility and secretion, which is, as a rule, lost in carcinoma, and normal in gastralgia. The pains of carcinoma as well as of ulcer increase on pressure ; in gastralgia they diminish on pressure, and in carcinoma we have anemia and cachexia as prominent signs. It has been said that the galvanic current, with 804 SENSORY NEUROSES. the anode on the epigastrium and the cathode on the spinal column, relieves the pain. These signs are not reliable, and as there is nothing typical about gastralgic attacks which should distinguish them from painful paroxysms issuing from other abdominal organs, we may say that, up to the present time, no pathognomonic sign or symptom of gastralgia exists. There are attacks of rheumatism and myalgia of the abdominal muscles which seem to become focused in the upper part of the abdomen, so that they may be confounded with gastralgic pains. Myalgic pains may occur from severe exertion of the abdominal musculature. These pains are increased by pressing or pinching the sore muscles ; they are not accompanied by any gastralgic symptoms whatever, are very much improved by rest, and, if they are rheumatic, by salol and salicy- late of soda. Intercostal neuralgias can be distinguished by the excessive and permanent sensitiveness to pressure which the affected nerves exhibit all along their course from the spinal column to the sternum. Cholelithiasis or the pains of an incar- cerated or passing gall-stone frequently irradiate so prominently to the epigastric region that they are more marked there than over the liver, but whenever the stone obstructs the ductus choledochus temporarily, the gall-bladder may be palpable by its dilation, and icterus and clay-colored stools are evident signs ; but in those patients in which the stone is impacted in the cystic duct and does not completely obstruct it, or rapidly passes through it, a differen- tial diagnosis is difficult, because the symptoms before mentioned are absent. But even in these cases great sensibility of the liver to pressure, anteriorly and posteriorly, is, as a rule, present. The liver is usually enlarged, and there is a painful point in cholelithia- sis at the twelfth dorsal vertebra, a few centimeters to the right of the spinal column. A careful search for gall-stone particles must be made in the passages. Gall-stones, as a rule, cause vomiting, while gastralgia rarely does so. The differential diagnosis between hepatalgia and gastralgia presents great difficulties. In nephritic colic the dyspeptic symptoms may be exactly like those of gastral- gia. The diagnosis between the two affections can be made with certainty by careful urinary examination for fragments of calculi and traces of blood, or by catheterization of the ureters in the inter- vals, and occasionally by localizing the renal calculus by the Ront- gen rays. (See Leonard, Chas. L., “ The X-ray Diagnosis, of Nephrolithiasis,” “ Phila. Med. Jour.,” vol. v, No. I, p. 50, Jan., 1900.) In intestinal colic the pains may be located in the upper TREATMENT OF GASTRALGI A. 805 part of the abdomen. They are mostly due to excessive gaseous distention of the intestinal loops, and are associated with consti- pation, and cease after the copious discharge of gas. Treatment. — In the treatment of gastralgia the fundamental cause must, if possible, be discovered and removed. In malarial districts the treatment by quinin and tonics is the most effective, if the causal relation can be established. Chlorosis and anemia should be treated by albuminate or peptonate of iron, ferratin, bone-marrow, arsenic, and highly nutritious diet. In some cases there is no better remedy than the tincture of the chlorid of iron. If the patient is an inveterate smoker, he must be cautioned to cease his habit. Enteroptosis, gout, and rheumatism must have suitable therapeutic attention. Disturbances of the genito-urinary organs, particularly of the female sexual organs, will command the attention of the specialist. Wherever we can find no cause for gastralgia, the only thing that can be done is to treat it sympto- matically. The most effective agent in our experience for this purpose has been the galvanic current. Large, felt-covered, copper plates are dipped in water as hot as the patient can bear it, the anode placed on the epigastrium and the cathode on the spinal column, extending from the cervical region downward between the scapulae. For this purpose we use very strong currents — not less than twenty-five milliamperes. Oser (“ Die Neurosen des Magens,” etc., Vienna and Leipsic, 1885) claims to have observed cessation of the pains after application of the faradic current. When the pains are not too intense, the internal administration of phosphate of codein, ^ of a grain every three hours, chloral hydrate, fifteen grains every two hours, Dover’s powder, tincture or extract of hyoscyamus, extract of belladonna, and camphorated tincture of opium are available remedies. Compound spirits of ether and the ethereal tincture of valerian, twenty drops every two hours, are useful when collapse is associated with the pain. Exalgin, antipyrin, and antifebrin have been recommended by Penzoldt. If the col- lapse is marked, wine, whisky, ether, and ammonia should be given until it has passed over. In pains of great intensity, the sovereign remedy is a hypodermic injection of ^ of a grain of morphin sul- phate, together with yq-q- of a grain of atropin sulphate injected directly into the epigastric region. Boas recommends suppositories of extract of opium and extract of belladonna. All of these agents are useful for the immediate treatment of a paroxysm ; they prob- ably have no curative effect on the underlying etiological trouble. 53 8o6 SENSORY NEUROSES. The irritability of the mucosa can be effectively reduced and gas- tralgic attacks sometimes altogether prevented from recurring by intragastric irrigation with lukewarm carbonated water (Malbranc, Kussmaul), or by treating the mucosa according to Fleiner’s method — with suspensions of bismuth subnitrate. We have seen excellent results from irrigations containing bismuth subnitrate (o i j ) , bismuth subgallate, 5ss in one pint of camphor water. The outflowing camphor water must be measured so as to ascertain that not over §j remains in the stomach. Although the pains of gas- tralgia are not influenced directly by the character of the food, the diet should be very bland and unirritating, and should not be taken in large quantities. Gastralgokenosis. — Under this name Boas describes a painful emptiness of the stomach which occurs one to two hours after meals, and may be so severe as to embarrass the respiration of the patient. The paroxysms last but one-quarter to one-half an hour, and are not connected with bulimia. These attacks are said to be relieved by the ingestion of milk, bread, etc. One of the cases of Boas developed into an attack every time he drank wine or cham- pagne or ate cake. We have never seen a case that corresponds to Boas’ description of this malady, and would suggest that it is probably a gastric hyperesthesia associated with hyperperistalsis and a strong secretion of HC1, particularly as the cases reported by Boas show that the reactions for HC1 were quite marked. ANOMALIES OF THE SENSATIONS OF HUNGER AND APPETITE . BULIMIA, OR HYPEROREXIA. Morbid increase of the sensation of hunger may occur as an independent idiopathic neurosis, as a result of abnormal irritability of the center controlling the sensation of hunger, or as a symptom of organic diseases. An intelligent insight into the pathogenesis of bulimia is possible only with a knowledge of the origin of the sensation of hunger. A modern physiological theory suggests that the hunger center in the medulla oblongata is stimulated nor- mally by the blood as soon as it has become impoverished in nutritive substances, and that the sensation of hunger ceases when the blood is saturated with nutritive substances. Stiller and others assert that the sensation of hunger results from excitation BULIMIA OR HYPEROREXI A. 807 of specific hunger nerves in the stomach, and that from here the sensation is conducted centripetally to the hunger center, and that, therefore, the normal sensation, as a rule, is brought to con- sciousness indirectly. Neither of these theories is supported by satisfactory clinical and experimental evidence. The appetite ceases when the stomach is filled with food, but that does not imply that the nutritive materials are already absorbed into the blood. This may require from three to four hours. In many gastric diseases the feeling of hunger is indirectly affected by the local disease, either increased or diminished. There are also general (metabolic) diseases which directly or indirectly increase or diminish the sensation of hunger. In some persons, even in the normal condition, vehement emotional excitations may cause a loss of hunger and appetite, although the blood is un- doubtedly impoverished in nutritive substances, so that we have clinical evidence sufficient to demonstrate a local, gastric, and a. remote or central nervous excitation of hunger. According to one hypothesis, hunger results every time the stomach becomes entirely empty, and Leo (“ Ueber Bulimia,” “ Deutsche med. Woch- enschr.,” 1889, Nr. 29 und 30) has asserted, in a most comprehen- sive report on this affection, that the abnormally rapid evacuation of the stomach is the cause of bulimia. This would naturally include that bulimia is very frequent with pyloric insufficiency, in which, as we know, the ingesta at once enter the intestine from the stomach. Bulimia should also then be frequent in cases where a gastroenterostomy has been executed for benign stenosis of the pylorus ; this is not the experience of the author with his cases of this class. Ewald and Fleischer have reported cases of bulimia in which there was no hypermotility. The combination of bulimia with hypermotility may possibly be explained by the fact that intense excitation of the hunger center may extend to neighboring centers in the medulla, and involve even the vagus center, which responds by affecting a more rapid evacuation of the gastric con- tents into the intestines. Some of the accompanying symptoms of bulimia (tinnitus and roaring in the ears, palpitation of the heart, and fainting) are attributed by R. Ewald (the physiologist) to sec- ondary irritation of nervous centers lying in close proximity to the hunger center. The affection expresses itself by violent sensa- tions of hunger coming on suddenly, even shortly after the com- pletion of a full meal, and if the desire for food is not immediately gratified, the patients exhibit signs of weakness, headache, pal- 8o8 SENSORY NEUROSES. lor of the face, palpitation of the heart, roaring noises in the ears, and gastric distress. The attacks may sometimes occur periodic- ally, but, as a rule, occur irregularly. In the intervals between the attacks hunger and appetite are normal, but there are cases in which bulimia may alternate with anorexia. Causation. — Bulimia may be an idiopathic, central neurosis con- nected with abnormal irritability of the hunger center, or a symp- tomatic affection which Leo (/. c.) has observed in exophthalmic goiter, with gastric ulcer and hyperacidity, chronic gastritis, tape- worm, diarrhea, and menorrhagia. It has been observed even with carcinoma and dilation. Fleischer states, without reserve, that the hyperexcitability of the hunger center is not caused by sudden and excessive impoverishment of the blood in nutritive substances, because the attacks may occur immediately after an abundantly nutritious meal which has brought about a feeling of satiety, and because, in other cases, the morbid sensation may be relieved by a mouthful of bread or a swallow of beer or wine. The fact that the sensations of hunger and thirst are normal in the intervals between the attacks, or even at times entirely absent, argues against the assumption that bulimia is always caused by a con- dition of the blood acting upon the central nervous system. The following are morbid conditions in which bulimia has been observed to occur : Cerebral tumors, epilepsy, psychoses, hysteria and neurasthenia, focal diseases of the brain, cerebral concussion, Basedow’s disease, Addison’s disease, tuberculosis, syphilis (accord- ing to Fournier, “Gazette Hebdom.,” 1871, No. 1—3, it occurs between the third and sixth month of this disease), diabetes mellitus, uterine disease, chronic gastritis, ulcer, dilation, car- cinoma, enteritis, and intestinal parasites. Bulimia has also been observed during the puerperium. Some authors classify the ravenous appetite following exhaustive continued fevers, as well as that following abundant loss of blood, with bulimia. This, in our opinion, is not a justifiable classification, because the increase of hunger in these cases can be explained in a simple and natural way without assuming a hypothetical excitability of the hunger center. In diabetes mellitus we may assume the existence of an abnormal irritability of the hunger center because these patients are not satisfied even shortly after large meals. It has been supposed that the glucose circulating in the blood is the agent that causes this irritation of the hunger center. In diabetic patients in which the sugar in the blood and urine has been reduced by a diet limited SYMPTOMS OF BULIMIA. 809 exclusively to fat and albuminous food, the torturing feelings of hunger disappear, to return again if the mellituria is allowed to increase on other diet. According to Pettenkofer and Voit, the metabolism of diabetic patients is much increased ; which, of course, means a more rapid consumption of the nutritive elements of the blood. The impoverishment of the blood is further augmented by the fact that the sugar which is formed from the amylaceous substances of the food is only partially or not at all utilized in the economy. The diagnosis of bulimia should only be made in diabetes if the violent sensations of hunger continue notwith- standing very rich and very abundant meals, or if it recurs very soon after such meals, by which the blood must have been charged with nutritive substances for a l.onger time. Ewald and Boas have observed that the attacks become less frequent after bodily exer- cise in the open air. According to Rosenthal, the affection is more frequent in women than in men, and occurs most often between the twentieth and fortieth years. Symptomatology. — The main and most characteristic symptom is the impulsive sensation of hunger, which by any and every means commands the ingestion of food. The pallor, weakness, and terror, with attacks of fainting and roaring in the ears, we have already described. This sensation comes on generally within one to two hours after meals, but it may occur within ten minutes after meals. We have known three old gentlemen who were for a long time aroused in the middle of the night by this torturing sensation of hunger. Some patients complain of gnawing and boring pain if the hunger is not gratified. Very small quantities of milk, beer, or wine, or only a few mouthfuls of cracker or bread, will cause the entire train of symptoms to disappear. Peyer (“ Correspon- denzbl. Schweitzer Aerzte,” 1888, Nr. 20) reports a case of a parox- ysm of bulimia occurring in a female patient when she was away from home visiting a friend. The weakness ensuing is described as having been so great that she could not return home. Peyer asserts that in three-quarters of an hour she consumed three pints of milk, twenty-three eggs, and two pints of strong wine before the bulimia and pain in the stomach ceased. The patient then fell asleep, and on awakening returned home perfectly well. Potton re- ports the case of a young, hysterical girl who was obliged to take eleven or twelve meals a day, and even eat during the night; she is claimed to have ingested between ten and twelve kilograms of food per diem, and was finally cured by gradually increasing doses 8io SENSORY NEUROSES. of morphin. This was a case of so-called continued bulimia. We have made studies of the dietary in two of our cases, a male and a female patient, and controlled the metabolism by determinations of the total nitrogen output in the urine and feces. The man took in food amounting to 7368 calories on an average, daily ; the woman consumed food to the value of 8131 calories. The curious obser- vation made was that both patients lost weight, and the stools con- tained from y to y? of the ingested food-stuffs in an undigested form. The female was not cured, but the man gave himself up to strict sanatorium management — his diet was gradually reduced to 2400 calories; under this food value he gained weight, and the urine contained less of toxic products than on his old bulimic food supply. Medicines were not used ; he was simply put under constant guard, day and night, by reliable nurses, and no more food allowed than was ordered by the physician. Diagnosis. — Wherever the abnormal sensation of hunger oc- curs shortly after abundant food has been taken, the diagnosis is not difficult ; at other times it may be confounded with polyphagia and acoria. In polyphagia the desire for eating is very much in- creased, but it does not occur until some time after the meals, and occurs gradually, not developing the intense hunger suddenly. So, polyphagia is simple increase of the normal sensation of appe- tite, such as we find in diabetes mellitus. It is impossible strictly to separate polyphagia from bulimia — both occur under similar con- ditions and as primary or secondary neuroses. Bouveret (“ Traite des Maladies de 1 ’Estomac,” Paris, 1893, page 654) refers to a case in which a patient seventeen years old could devour 100 pounds of meat in twenty-four hours, and Rosenthal reports an instance of a woman, aged twenty-eight years, who ate at one meal a whole roast of goose and a large portion of bread. There is a so-called continued form of bulimia which alternates with acoria, or the absence of the feeling of gratification or satisfaction after meals. If it can be found that the feeling of hunger is very great, and even continues or returns after abundant meals, then we are dealing with bulimia; but if the sensation of hunger is normal or reduced, and ceases after larger meals, but without causing the feeling of satiety, we are dealing with acoria. The continued form of bulimia has hitherto been found only with diabetes mellitus and hysteria. We have had two cases in hospital practice which illustrate that bulimia and polyphagia may be developed by practice. Both cases occurred in negroes who had, as a result of a number of wagers. ACORIA. 8 1 1 eaten large quantities of food. One colored man was a waiter at a hotel at Cape May, N. J.,and made a practice of exhibiting himself by eating a huge watermelon together with eight pies. The other negro, who was a patient at Baltimore, gradually developed his polyphagia from participating in rival encounters with other individuals of his race to see who could eat the most oysters. It is claimed that this man could eat three quarts of oysters, with a large amount of crackers and beer. Both negroes found later that the habit had developed into a disease, the tremendous appetite developing very often within a half hour after the big meals of bread, fish, and egg had been taken. One of them has been cured by dram doses of bromid of ammonia four times daily. The diagnosis of an affec- tion of this character can not be stated in such exact terms as that of an organic disease, as individual opinions of specialists as to what really constitutes bulimia will probably vary greatly. (The treatment will be considered together with that of acoria.) ACORIA. This word is derived from « and %opiwufu, I become satiated. “Acoria ” denotes the absence of the normal feeling of satiation, even after very abundant meals, without increase of hunger or appetite. Acoria is not identical with bulimia or polyphagia, for in both of these there is a very strong feeling of hunger, while in acoria we may have absence of appetite. Even in polyphagic gluttons the feeling of satiation will eventually supervene, but not in acoria. The disease is generally secondary to neurasthenia, hysteria, and certain psychoses. It is occasionally met with in sexual neuras- thenics. The feeling of satiation is no positive sensation ; it occurs when hunger and appetite have been appeased, and is therefore a negative sensation. Hunger and appetite cease normally when the hunger center passes from a sensation of excitation to that of rest. The amount of food required to accomplish this varies greatly in different persons, and even in the same person at different times. One hypothesis has attempted to explain acoria on the basis of overexcitation of the hunger center. If this were the case, we would find, periodically at least, an increased sensation of hunger after large meals, which is never observed in acoria, for hunger and appetite are normal, or even subnormal, in acoria. Some patients even state that after meals hunger ceases, but they SENSORY NEUROSES. have no feeling of satiation ; in fact, no impression whatever from the stomach informing them that they have eaten enough. It is well known that many people are not satisfied to introduce food until the appetite has been appeased, but they continue long enough to perceive a feeling of pressure and slight fullness in the stomach, which is a result of a moderate distention of the gastric walls by ingesta. While moderate eaters perceive this sensation as uncomfortable and indicating supersatiation, gormandizers gradu- ally become accustomed to this feeling of pressure and fullness, sometimes from early childhood, so that eventually they do not believe themselves satiated before this distention occurs, and this fullness and distention are finally confounded with the normal sen- sation of satiety. The next step in the development of this nervous anomaly is that the feeling of pressure and fullness may mimic a temporary normal feeling of satiation, while at the same time the excitation of the hunger center continues. The sensation of hunger, when it is not very strong, may be in some cases removed by filling the stomach with perfectly indigestible material, such as leaves and sawdust. In the voyage of the Jeanette (Journal of Lieutenant de Long, commanding the expedition, 1883) the crew of the sur- viving members subsisted upon scraps of deer skin, which, from its bulk in the stomach, seemed to afford relief from hunger. After everything was exhausted they lived upon an infusion made from arctic willow, containing really no nourishment, and ate two old boots. As the feeling of satiation is absent after copious filling of the stomach with food, and as it can not be disguised by an abnormal feeling of hunger, because hunger is normal or sub- normal in acoria, another explanation that has been offered for this nervous affliction is that it is due to loss of sensibility, or anesthesia, of the gastric sensory nerves. This seems to be a very probable explanation, since we have personally had at least one experience that would suggest a local gastric anesthesia as an ex- planation of acoria. The case we have in mind is that of a young woman whose stomach we had sprayed with a three per cent, solu- tion of cocain and menthol. She returned on the same day, stating that, although she had taken a long bicycle ride after the spraying, and returned home feeling quite hungry, she had the impression that the food she ate never reached the stomach. She had no feel- ing in her stomach that the meal effected satiation. At first we overlooked the causal relation between the spraying with menthol NERVOUS ANOREXIA. 813 and cocain for this temporary acoria, and our attention was attracted to it after the same symptoms were complained of each time the menthol and cocain were used. These agents had been employed for the relief of gastralgic pains resulting from erosions. The case ultimately recovered by treating it with suspensions of sub- nitrate of bismuth. It is conceivable that anesthesia of the stom- ach nerves may occur from repeated overdistention, as occurs in bulimia, polyphagia, diabetes mellitus, and dilation of the stomach. Symptomatology. — As the only symptom is the absence of satiation, the clinical picture is not very manifold. The complaints of the patients are limited to the statement that large meals cause no sensation of having had enough to eat, and that they do not know when to cease eating; that they have to measure out their food previous to beginning to eat, in order to know when they have had sufficient. Some of these patients try to compel a feeling of satiation by the ingestion of enormous quantities of food and drink. This has been reported as a cause of gastritis, atony, and dilation. The prognosis varies according to the fundamental disease. The diagnosis is made from the single important symptom and the exclusion of bulimia and polyphagia. Sometimes we find transitions from acoria to bulimia, which Boas explains by a reac- tive hyperesthesia following an anesthesia of the gastric nerves. Acoria is distinguished from polyphagia by the increased desire for food, which is marked in the latter, very likely as a result of increased oxidation, while the diagnosis from bulimia hinges upon the raven- ous desire for food in the latter; in both the feeling of satiation will eventually supervene. Treatment. — The treatment of bulimia when it is a secondary disease must have regard for removal of the primary cause, such as intestinal parasites, genito-urinary diseases, hyperacidity, or ulcer, and any existing neurasthenia, hysteria, or psychosis. The bromids are very valuable remedies to reduce the irritability of the hunger center ; they should be given in the form of bromid of ammonia or strontium, thirty grains of either four times a day, preferably in peppermint water. The following formula will be found useful in bulimia: B. Tinct. opii camph., 81.0 f^iij Tinct. belladonna, 1.0 gtt. xl Elix. simplic., q. s. 180.0 f^vj. M. Sig. — O ne-half of a fluidounce three times a day. 814 SENSORY NEUROSES. Arsenic, in form of Fowler’s solution, beginning with three to five drops, and gradually increasing the dose to ten to fifteen drops, is highly recommended by Boas. Rosenthal recommends subcu- taneous injections of extract of opium, and has seen good results in bulimia from cocain hydrochlorate. Morphin is a remedy that has been followed by good results in this affection. An attempt should be made with the use of electricity in the treatment. In one of the colored patients to whom we referred as champion gluttons, and who had subsequently developed bulimia, the symptoms im- proved very much under the intragastric use of the constant current. The treatment of acoria should be mainly that of neurasthenia ; climatic changes and electrical hydropathic cures are most effec- tive. Intragastric douches, with alternating warm and cold water, have been recommended. It is very important that these patients should be watched by healthy friends during their eating ; thorough mastication and insalivation should be insisted upon. Strychnin and massage of the stomach suggest themselves as rational means of treatment. NERVOUS ANOREXIA. By anorexia is meant an entire absence of appetite and loss of the sensation of hunger. The superlative degree of this sensation is expressed in the disgust and repugnance toward all food. There are probably no pathological conditions, neither of the stomach nor of any other organ of the body, in which anorexia is not occasionally met with. In most anatomical diseases of the stomach anorexia is a regular accompaniment. The separation of appetite and hunger is not so clear as one might suppose ; the two are not necessarily synonymous, nor does one include the other. Penzoldt defines hunger as the warning or admonition, and appetite as the pleasure of eating (“ Bibliothek der ges. medizin. Wissenschaften, heraus- gegeben von Drasche,” article on “ Anorexia ”). There may even be appetite when there can not possibly be hunger. We have already spoken of the various forms of anorexia that may accompany the organic and functional diseases of the stomach. By nervous ano- rexia we mean loss of appetite, and even repugnance to food, that may extend over weeks and months, with a perfectly intact diges- tive apparatus; this affection is found principally in women, and is based upon neurasthenia, hysteria, anemia, chlorosis, and certain neuroses of the stomach. It is found in those addicted to the excessive use of alcohol and tobacco, and as a symptom of the TREATMENT OF ANOREXIA. 815 morphin habit. It is, therefore, not a disease peculiar to itself, not a typical morbid entity, but rather a sequence. Whether or not nervous anorexia may be an independent disease of central origin, a neurosis connected with a reduced irritability of the hun- ger center, has, up to the present time, not been satisfactorily investigated. The course and the prognosis depend upon the degree of the repugnance for food. Among the insane and very neurasthenic patients fatal cases have been reported. Symptomatology. — The patients who, from loss of appetite or distress, can not take food, grow anemic and weak, appear very emaciated, have a slow, feeble pulse, cold hands and feet, and may even give the impression of tuberculous patients. Rosenthal (“ Magenneurosen,” etc., Vienna and Leipzig, 1886), Gull (“The Lancet,” 1868), and Charcot (“Oeuvres Completes,” tome ill, p. 240) have reported fatal cases of nervous anorexia. Insomnia is a frequent symptom of this affection. Very slight anatomical changes in the stomach may cause anorexia ; it is, therefore, almost impossible to make the diagnosis of secondary or primary anorexia with precision. Diagnosis. — There is no difficulty about the diagnosis of anorexia, but it is not always easy to discover the real cause of it. We will find under the consideration of enteroptosis that almost any abdominal organ when dislocated may produce this symptom. Organic affections of the stomach must be excluded before we can make the diagnosis of nervous anorexia. Very frequently chronic gastritis, incipient tuberculosis, and carcinoma begin with this symptom before any other signs or symptoms are manifest. Treatment. — The primary object of the treatment must be to improve the general nervous condition, to correct any exist- ing fundamental disease, to act upon the psychical sphere by per- suasion, suggestion, and firm but kind argument, and, finally, to combat the anorexia itself directly. Any existing neurasthenia and hysteria should be treated by methods that have been spoken of repeatedly for these affections. Dujardin-Beaumetz (“Traite- ment des Maladies de l’Estomac,” 1891, p. 326) speaks very highly of arsenic in the treatment of nervous anorexia. In anemia mild preparations of iron (see ferratin) are almost indispensable. The tincture of the chlorid of iron and the Blaud pill will rarely disagree, and in those cases in which these forms produce gastric distress I found that organic mixtures of iron did so likewise. (See Hem- meter, “Absorption of Iron from the Gastro-intestinal Tract,” etc., 8i6 NEUROSES OF SECRETION. “ Phila. Med. Jour.,” January 13, 1900.) It has been found that iron injected subcutaneously will produce dyspeptic distress (Glaevecke, “Arch. f. experim. Path. u. Pharm.,” 1883, Bd. xvn). This effect of iron in rare cases is unavoidable and not well under- stood. In order to improve the general nutrition, the Weir Mitchell rest-cure, — which consists in isolating the patient from his family and placing him under the supervision of a trained nurse and an experienced physician, and feeding him so abundantly that gradually a gain of weight is accomplished, — together with the use of baths, massage, and electricity, has, in many cases in our experience, produced happy results when other means have failed. When there is an absolute repugnance for food, or when the patient is insane, artificial compulsory alimentation by gavage should not be postponed too long. We have considered this fully on page 190. In the beginning of the trouble the bitter tonics are available to stimulate the appetite. The basic orexin, five to ten grains three times a day, in a cup of hot bouillon, produces some- times excellent results in these cases of nervous loss of appetite. Boas speaks very highly of the cinchona bark. It may be pre- scribed in the following formula : R. Tinct. cinchonse comp. 40.0 f!|iss Acid, sulphuric, dil. , io.o f^ij Syr. zingiber., q. s. 240.0 f|jvj. M. SlG. — One-half of a fluidounce in two ounces of water, through a glass tube, three times a day. In some cases in which the anorexia was due to a feeling of pressure and discomfort after eating, Rosenthal reports good results from ten to fifteen grains of bromid of sodium given before meals. Boas cautions against the use of mineral waters in the treatment of this neurosis. One most approved combination for anorexia is given on page 571 ; it contains dilute HC 1 , because I have found, in a very large number of cases of intense nervous anorexia, that the gastric secretion is very much deduced or entirely lost, and I have rarely observed persistent anorexia together with normal HC 1 secretion. SUPEKACI DITY. Si/ CHAPTER XII. NEUROSES OF SECRETION. HYPERCHYLIA (Hyper- or Superacidity; Hyperciilorhydria). Most diagnosticians whose clinical and laboratory experience renders them competent to judge, consider hyperacidity and hyper- secretion of the gastric juice to be neuroses of the secretory func- tion. They are regarded as functional disturbances of the nerves of the stomach, which may occur as individual diseases or as part of other neurotic conditions. This view no doubt is correct in a large number of the cases. It includes the opinion that in this dis- ease no characteristic changes in the structure of the gastric mucous membrane are demonstrable. Judging from the results of Hayem, Cohnheim, and Einhorn, and the author,* it is beyond a doubt that in more than one-half the cases of hyperacidity ex- amined, proliferation of the glandular elements is present. I have not only examined fragments of mucosa that were accident- ally found in the wash-water, but have had opportunities of making autopsies on cases of pronounced and prolonged hyperacidity that died of intercurrent diseases. In serial sections of these stomachs it was found that the prevailing state of the mucosa in the inter- mediate zone and fundus was that of glandular proliferation, with increase in the number of oxyntic cells. Such stomachs do not show the same conditions throughout. On making serial sections of large pieces of the secretory portion, one occasionally meets with areas in which the glandular structure is apparently normal. At very rare intervals and in rare cases one can even find sections showing partial glandular atrophy. This is so rare as to be insignificant. Even in normal stomachs one sometimes finds indi- cations of atrophy in serial sections, and we consider that these changes are very limited, and, perhaps, may be considered as pro- cesses of reconstruction and transition, where accidentally injured or exhausted glands break down in minute foci and are replaced gradually by newly formed gland-cells. The prevailing condition, * Hemmeter, “ Z. Histologie d. Magendriisen b. Hyperaciditat,” “ Archiv f. Ver- dauungskrankheiten,” Bd. IV, S. 23. 8 1 8 NEUROSES OF SECRETION. then, in hyperacidity, according to our opinion, is proliferation of the glandular elements and increase of oxyntic or border cells. A large number of microscopical investigations will be neces- sary to confirm this opinion. I have thus far examined the entire stomach of four cases that gave the clinical picture of hyper- acidity before death. In all four of these cases the proliferation of the glandular elements was uniformly present. Strauss has de- scribed conditions in the gastric glandular layer which are con- firmatory of my own results (“ Virchow’s Archiv,” 1898, Bd. cliv). Sir William Roberts (“ Digestion and Diet,” p. 240) holds that the acid in what he calls acid dyspepsia (which seems to me an objec- tionable term, since it does not define which of the diseases that are connected with excess of acidity he refers to) is not unmixed HC1, but that lactic, butyric, tartaric, and malic acids are present. These are probably derived from salts of the organic acids present in articles of food which are decomposed by the HC1 of the gas- tric juice. There may, of course, be a hyperacidity due to excess of organic acids, which may present all the symptoms of hyper- chlorhydria; in such cases there is, in my experience, no HC1 secreted at all. What I refer to clinically as hyperacidity, how- ever, is an excessive formation of hydrochloric acid from the gas- tric glands. Concerning the nature and origin of this acid we have nothing but theories. It has been suggested that the hyperchlorhydria is due to an excess of chlorids in the organism, from which it liberates itself by excretion into an organ where the freeing of the system from chlorids could at the same time become of utility as a digestive secretion in the form of HC1. The author has made a number of experiments by feeding carnivorous animals with food from which the chlorids had been removed so far as was possible. The acidity of the gastric juice of the dog will become very much reduced if the chlorids are withdrawn from the food. This, however, is no proof of the supposition that the reduction of chlorids is the cause of the diminished secretion of HC1, because foods containing consider- able of chlorids are a healthy stimulant to the normal secretion of HC1, and food deprived of chlorids can not exert this stimulation upon the mucosa. Personally, the author considers it very probable that hyperacidity is frequently an adaptive process : that is to say, the glandular layer gradually develops greater secretory powers, because more secretion of HC1 is required by the nature of the ingested food. We have been told by two physicians practising in RELATION OF ACIDITY OF URINE AND GASTRIC ACIDITY. 8 19 Japan that hyperacidity, as well as gastric ulcer, are practically unknown in that country, which may be partially explained by the exclusive carbohydrate diet upon which the middle and lower classes of that nation exist. It is a well-known fact that the gastric juice of carnivora contains relatively more HC 1 than that of the herbivora. It may not be so well known that the gastric juice of a carnivorous animal can be made to contain a less amount of HC 1 by being fed upon a carbohydrate diet for a long time. Two dogs of the same litter, (a), fed exclusively on milk, potatoes, and rye bread, and (£), fed exclusively on beef, mutton, pork, fish, and water: At the end of one year dog (a), fed upon carbohydrates, had a gastric juice one hour after a roll and a half pint of water, containing 3 per 1000 of HC 1 ; dog ( b ), who was fed upon a meat diet, had a gastric juice containing 6.540 per 1000 HC 1 after the same test-meal. The figures are the results of the aver- age of ten different analyses on each dog. These two dogs were raised in two entirely different families. Dog (a) was raised by a gentleman living in a country district where meat was not easily ob- tained and milk was very abundant ; dog ( b ) was raised in the city, and lived upon the refuse meats from the table. Since the publica- tion of the first edition these two fox terriers have been kept in the same families and two other terriers have been raised in the same way. The results of test-meals showing that the gastric juice of the dogs raised on meat contains twice as much HC 1 on the aver- age (6.6320 per 1000) as that of the dogs fed on milk, bread, and potatoes. Unless conducted in this manner, and watched by com- petent observers for a long time, — at least one year, — the experi- ment is of no practical utility. It is conceivable that we do not as yet know all of the constituents of the gastric juice ; clinically, it has been very frequently observed that the secretions of the intes- tines may contain traces of products of metabolism and other toxins when the function of the kidney is suppressed or lost. The gastric j uice of epileptics may contain toxic substances. Augustini, who recently investigated this subject, found that the gastric juice of an epileptic, when injected into the abdomen of a rabbit, proved fatal, with general toxic symptoms and clonic convulsions. This was especially true when the gastric juice was obtained immediately before or after an attack. Normal gastric juice was found to pro- duce no such evil effects. The probable action of bacteria can not be excluded from these experiments. Augustini concludes from these experiments that systematic lavage and disinfection of 820 NEUROSES OF SECRETION. the stomach and intestines are indicated in all cases of epilepsy. What we wish to emphasize in this introduction to the considera- tion of hyperacidity is that hyperchlorhydria, although frequently a neurosis, is, in our opinion, very often a process of adaptation of the mucosa to the demand for increased work. Acidity of the Urine and Gastric Contents in the Healthy and in the Dyspeptic. — Mathieu and Treheux (“ Arch. Gen. de Med.,” November, 1895) have made researches on this subject. They examined the urine hourly during the afternoon, after the midday meal, carrying out their investigations on twelve persons, after eighty-four different meals, thus making over 400 estimates of the degree of acidity of the gastric contents and urine. The individuals examined were the subjects of hyperchlorhydria, with and without symptoms of gastric dilation, carcinoma, etc. The authors conclude that : (1) There is a relation between the acidity of the gastric contents and the urine. (2) The greater the production of acid, whether by secretion or fermentation, the greater the amount of acid excretion in the urine. (3) Normally, the acidity of the urine falls during the first three to five hours after eating; thereafter it increases. (4) Most often there is an almost absolute parallelism between the two curves of gastric and urinary acidity, but this is destroyed after a repast by the presence of polyuria. (5) If the acid is withdrawn by any means from the stomach, the amount in the urine falls also, and the latter may even become alkaline. (6) The average quantity eliminated by the urine hourly is greater in hypochlorhydria (subacidity) than in hyperchlorhy- dria (superacidity). (7) Milk increases the acid in the urine, owing to its giving rise to lactic acid in the stomach. (8) It is not possible, at any rate at present, to trace the curves of urinary acidity so as to bear indirectly on the question of the chemical variety of the dyspepsia. (9) Milk must be excluded from test- meals when these curves are to be studied. (10) Patients should be subjected to a constant regimen for some time before the in- vestigations. Nature and Concept. — As the name implies, the factor with which we are most particularly concerned in this neurosis is the HC 1 . With superacidity, a gastric juice unusually rich in HC 1 and pepsin is secreted in very large quantities during digestion, as a result of the stimulation of the foods. On this account free HC 1 may be proved in the stomach after test-meals much earlier than under normal circumstances, and the acidity of the digestive HISTORY OF SUPERACIDITY. 821 mixture is further increased as digestion proceeds. Superacidity may be an independent disease confined to the stomach alone, or a partial symptom of hysteria, neurasthenia, and melancholia. It may also be noticed as a reflex neurosis with renal calculus and hepatic colic, and as the companion of organic changes of the stomach (ulcus ventriculi, gastritis acida). Historical. — Even if superacidity, like supersecretion, has been demonstrated with certainty only in the last twelve years, through the researches of Reichmann, Jaworski, van den Velden, Riegel, the latter’s pupils, and others, and the aspect of the disease has been precisely defined by them, nevertheless, as Ewald justly em- phasizes, it would be an error to believe that we have to do with an entirely new discovery, since both these anomalies of secretion, as also their nervous origin, were known to older physicians in the beginning and middle of this century — men celebrated in England, France, and Germany (Trousseau, Todd, Budd, Copland, Pem- berton, Hiibner, and others). By some of these, the most impor- tant symptoms were also correctly stated. It is not intended that the merit of the previously mentioned investigators of these neu- roses of secretion shall be in any way diminished by this older historical reminiscence, for as the older physicians, owing to the lack of exact methods, could not recognize those anomalies of secretion with certainty, their results were soon forgotten ; Reich- mann was the first who, by a thorough examination of the contents of the stomach, with the help of newer and constantly improving methods, furnished certain proof of the existence of secretory dis- orders which had previously been only suspected, while it was Ewald especially who emphasized particularly the nervous origin of supersecretion and superacidity, so that soon they were generally recognized as neuroses. The observations of Reichmann were soon after confirmed by von Noorden, Honigmann, Riegel, Ja- worski, Saly, and others, and to-day there is a consensus of opinion concerning the nature and consequences of both neuroses. Jaworski designates both neuroses as very frequent disorders, since he could prove them in almost two-thirds of his patients who had diseases of the stomach, while Riegel also observed them very frequently in Hessia, — although not quite so frequently as Jaworski, — Ewald, with whom the author can agree, states that they, especially super- secretion, occurred only in a fraction of his patients with diseases of the stomach, so that supersecretion should be called rare, rather than frequent. 54 822 NEUROSES OF SECRETION. Etiology. — The fundamental causes of superacidity are still unknown. The little that has up to date become known con- cerning the etiology of the disease is confined to the knowledge of a few predisposing factors. Very excitable people, predisposed to nervous disorders, more frequently become affected with super- acidity than those of calm temperament, who do not lose their equanimity so easily, although it is not found entirely wanting in the latter. Jaworski found hyperacidity very frequently in the excitable Jewish population of Galicia, preeminently disposed to nervous disorders. With hysterical patients superacidity was noticed by Jolly, and in melancholic subjects by von Noorden, and it is also a frequent companion to neurasthenia. The disease is more common in men than in women. The educated, and particu- larly the learned, classes furnish the main body of patients suffering from superacidity, though it is not infrequent in the laboring classes. Local causes seem to play an important role in the etiology of superacidity, and this is vouched for by the frequent occurrence of the disease in Galicia and Hessia (Riegel), while it is much rarer in other districts. It would be a valuable contribution by various gastro-enterologists of the United States if they collected and re- ported the frequency of hyperacidity and other gastric diseases occurring in their localities, so as to throw light on the influences of race, climate, geographical distribution, etc. It is my opinion that a diet rich in fish, meats, and proteids in general predispose to hyperacidity. That the frequent occurrence of superacidity with cholelithiasis and nephrolithiasis is a causal relation and not a mere accidental coincidence is shown by the fact that the stomach com- plaints dependent on superacidity generally disappear quickly after the passage of the calculi into the intestines and bladder respectively. The relation between superacidity and peptic ulcer has been suffi- ciently dwelt upon in the discussion of the pathogenesis of the latter ; whether superacidity is a cause or result of the ulcer, it has, up to date, been impossible to decide with certainty. In the first half of this work the author has laid down reasons why hyperacidity may in some instances be sufficiently explained by the proliferation of glandular elements observed in fragments of mucosa found in the wash-water in one-half to two-thirds of the cases of hyperacidity examined (Hemmeter, “ Experimental Basis of the Dietetic and Medicinal Treatment of Hyperacidity,” etc., “ Jour. Amer. Med. Asso.,” Oct. 9, 1897). Whether this condition is the cause or the SYMPTOMATOLOGY OF SUPERACI DITY. 823 result of the neurasthenia is difficult to determine, though we ob- served it when no neurasthenia could be detected. Symptomatology. — Disturbances of Sensibility . — The subjective complaints consist chiefly in contracting, boring, burning, or gnawing pains in the entire region of the stomach, which generally radiate forward or toward the back. As they are the consequences of a strong irritation of the mucous membrane of the stomach by its superacid contents, they are generally noticed only during digestion, appearing some time after eating, and generally increasing perceptibly with the progress of digestion. They are much influ- enced by the quantity and composition of the food; with meats they are in some patients less perceptible than with an amylaceous diet. After the introduction of food very rich in albumin they ap- pear later than with a diet poor in albuminates, mainly because in the former case the appearance of free HC1 in the contents of the stomach is postponed because the first HC1 that is secreted combines with the albumen. At the height of digestion the symp- toms are generally most severe. Temporary, strong, cramp-like pains in the region of the pylorus are generally the result of a spasm of the muscular sphincter of the pylorus. By alkalies, as also by the renewed taking of milk, eggs, or meat, the painful sensations are generally soon alleviated or temporarily done away with, so long as the acid is held in combination by the alkalies or albuminates. If a strong generation and collection of gases occur, the region of the stomach is swollen, and in some degree sensitive to touch. If the escape of the gases upward or downward is temporarily prevented by simultaneous cramp of the cardia and pylorus, the complaints are considerably increased, owing to the strong expan- sion of the walls of the stomach. Other gastric symptoms, such as nausea, belching, and vomiting of very acid masses accompany hyperchylia very frequently. Belching effects slight, passing relief, while copious vomiting brings greater and more lasting relief. If small quantities of the very acid contents of the stomach are brought up through the eructations, and if the mucous membrane of the esophagus is subjected to caustic action by the latter, heart- burn develops, which may increase to a severe contracting pain under the sternum, which extends to the pharynx (pyrosis hydro- chlorica, Sticker). The same complaints, naturally, may also appear after the vomiting of the contents of a very acid stomach. The manifold subjective symptoms previously stated are sometimes also observed with neurasthenic patients in whom the acidity of 824 NEUROSES OF SECRETION. the gastric juice is normal. An abnormal sensibility of the gastric nerves to hydrochloric acid must be supposed in these cases (Talma). The appetite is generally undisturbed in patients afflicted with superacidity; occasionally, it is even increased. Thirst is often much increased. The Influence of Hyperchylia upon the Transformation of the Foods in the Stomach. — As is well known, with increasing acidity of the gastric juice (at least, up to a certain limit) its digestive power for albuminous foods is increased, and peptonization proceeds more quickly and freely the sooner free hydrochloric acid is present in the contents of the stomach. Both conditions are given with patients suffering from hyperacidity. The acidity of the gastric juice is much greater than that of the normal secretion, which amounts to 0.15 to 0.2 per cent. It varies between 0.3 and 0.6 per cent, in hyperchylia; in severe cases between 0.4 and 0.6 per cent., so that in these 80 to 120 c.c. of a decinormal solution of sodium hydroxid are necessary to neutralize 100 c.c. of the gas- tric contents drawn at the height of the digestion of a test-meal. Free HC 1 may be shown in the contents of the stomach in ten minutes after a test-breakfast, instead of in an hour, and in one hour, instead of in three to four hours, after the full test-dinner ; therefore, the peptonization of albumin proceeds in a very prompt and free manner. On the other hand, gastric amylolysis is some- what retarded, as the effectiveness of the ptyalin is interrupted very early by the appearance of free HC 1 . On this account one finds, in three to four hours after an experimental meal, no undigested mus- cular fibers and albuminous particles in the contents of the stom- ach ; but many unchanged amylaceous particles may still be found in the residue on the filter. (This is best studied with the double test-meal, as recommended on pp. 120, 121.) If the acidity of the gastric juice exceeds a certain maximum (0.6 to 0.7 per cent, and over), even the digestion of the albumin is in some way retarded (Schwann), due, in my opinion, to an unusually large amount of peptone present. Ferments do not act readily in the presence of an excess of their products. But up to the present time such great quantities of free HC 1 have not been met with in the contents of the stomachs of patients suffering from hyperacidity. A copious formation and collection of gases may occur in this neurosis of secretion. The Effect on the Motor Function. — With very severe irritation THE EFFECT ON THE MOTOR FUNCTION. 825 of the mucous membrane of the stomach by the overacid contents, abnormally severe contractions of the musculature are produced reflexly, by which a quicker flow of blood to and from the gastric walls is effected. A more intimate contact of the ingesta with the mucous membrane of stomach hastens secretion as well as the digestion and resorption of the albuminates, and also the passing over of the chyme into the intestines. Therefore, one should ex- pect a quickened emptying of the stomach in patients with hyper- acidity ; but in many cases exactly the opposite is noted — namely, a retarded passage of the contents of the stomach into the intestines. It is generally caused by a stubborn, often-recurring cramp of the pylorus, brought about by the strong irritation of the mucous membrane of the pylorus by HC1, which even the most extreme contractions of the rest of the musculature can not overcome. These overexertions of the latter may lead to fatigue and to atony, and the appearance of this state is furthered by the fact that the coats of the stomach are burdened and distended by the ingesta more than under normal circumstances. Since, however, the musculature can rest and recuperate with an empty stomach, the atony does not very frequently pass over into a chronic state of dilation of the stomach. The formation of the dilation is, how- ever, to be feared when the cramp of the pylorus brings about a hypertrophy of its ring muscles, and with it a stenosis of its lumen. The disturbances of circulation in the coats of the stom- ach, caused by the cramp of the pylorus, in the presence of a very acid and potent gastric juice may favor the formation of peptic ulcer. The troublesome thirst so often complained of by patients was formerly explained by a reduction of the power of resorption of the mucous membrane, caused by the strong irritation of the same (HC1) and spasm of the smaller vessels. The quick cessa- tion of thirst after copious drafts of water has been explained by the dilution of the acid chyme and a decrease of the irritation of the mucous membrane. That superacidity may cause disturbance of resorption is not to be denied. Since it is known, however, that the greater part of the water introduced is absorbed only in the intestine, and that the resorption of water in the normal stomach is only very slight, it might be more correct to trace back the thirst with superacidity to the cramp of the pylorus and the longer retention of the water in the stomach. After copious drinking of water, with dilution of the contents of the stomach, the irritation of the mucous mem- 826 NEUROSES OF SECRETION. brane of the pylorus decreases, the cramp is lessened, and the water, passing into the small intestine, is then quickly absorbed in the latter. That, indeed, a cramp of the pylorus with hyperacidity often causes retention of the contents of the stomach may be proved by the introduction of the tube before and after taking the water — especially when it contains alkalies (Saratoga Vichy). Before the taking of water the contents of the stomach still show abundance of food ; while some time after, the stomach is generally found to be entirely empty. Urine . — After copious vomiting, by which a part of the HC1 is permanently removed from the organism, the urine has an alkaline or neutral reaction (Sticker, Gluzinski, Jaworski, and Hiibner); but this may be observed during the digestion in the stomach without vomiting. Since the phosphates more easily separate out of the alkaline urine, it may happen that the urine is turbid or milk- like when voided, a circumstance sometimes unnecessarily alarm- ing the patient ; or, after standing a while, the urine may show a very plentiful sediment. The chlorids are sometimes decreased. The state of nutrition generally remains good, especially at first. If considerable disturbance of the motility appears, the nutrition becomes impaired. The Digestion of the Foods in the Intestine . — If the contents of the stomach enter the intestine in an overacid condition, it requires much more than the usual time to attain the alkaline reaction in the contents of the intestines with the help of the mixed alkaline intestinal juices. An alkaline medium is the most favorable for the digestion of fats and carbohydrates. In the period immediately succeeding the passage of the chyme into the small intestine, so long as there is still free HC1 present, a small part of the undigested albumin is peptonized by the pepsin which has passed over along with it, while, on the other hand, the transformation of the carbohydrates and fats is arrested in this time. Consequently, the digestion and assimilation of the foods in the intestine are much retarded in severe cases of hyperacidity, and the evacuation of the bowels is correspondingly delayed. The very acid chyme occasionally produces an abnormally intense peristalsis of the intestine, so that in exceptional cases the evacu- ation of the intestines may be diarrheic in character. Prognosis. — This is favorable if the disease is of recent origin ; older cases, however, are often stubborn. The ever- recurring pains and disturbances of digestion may, in the course of time, exhaust DIFFERENTIATION OF HYPERACIDITY FROM ULCER. 827 the patient. With symptomatic superacidity the prognosis must be made in accordance with that of the primary complaints. If these — e. g ., hysteria, neurasthenia, melancholia, peptic ulcer, or cholelithiasis and nephrolithiasis — are successfully relieved, the superacidity will quickly disappear. In the author’s experience per- manent relief may follow persistent treatment, even in chronic cases. Diagnosis. — In this disease our double test-meal (see p. 1 2 1 ) is a special diagnostic aid. If a strong reaction for HCl is shown in the contents of the stomach after ten to twenty minutes succeeding the test-breakfast, or in one to one and one-half hours after the test- dinner, and if the macroscopic and microscopic examinations in the residue on the filter still show abundant remnants of carbohydrates, with complete absence of muscular fibers and particles of albumin, then the diagnosis of hyperacidity is established, even though the other previously mentioned symptoms may be absent. In order to prove or disprove a coexistent supersecretion, we recommend to let the patient take the test-meal at night, and the next morning introduce the tube before breakfast. If it contains large quantities (over ioo c.c.) of a potent secretion, then supersecretion exists side by side with superacidity; and if the stomach be empty, or if only a small quantity of gastric juice be found in it, then superse- cretion is not present. The result is still more certain if a few hours after the last evening meal the stomach is thoroughly washed out and the tube is introduced into the jejune stomach the next morning. Schreiber asserts that supersecretion is found only in atonic stomachs. The differential diagnosis between the ulcer and hyperacidity is of practical importance on account of the therapeutics to be fol- lowed. With both diseases the manifold subjective complaints appear usually after eating ; with peptic ulcer patients, generally very soon after eating ; with those suffering from hyperacidity, later on at the height of digestion, though the onset varies considerably according to the quantity and character of the foods. In gastric ulcer the pains are generally confined to one region, — namely, the epigastrium (circumscribed pain caused by pressure), — and they very often radiate forward, laterally, toward the loins and shoulder-blades (dorsal pain-points), while in the case of super- acidity a diffused sensation of pain exists in the whole region of the stomach and the radiating pains are wanting, and also the dorsal pain-points, which, in the case of ulcer, will be present in about one-third of the cases. 828 NEUROSES OF SECRETION. In the case of ulcer the pains are generally strongest when food in itself difficult of digestion has been introduced in large quanti- ties, and it is irrelevant in this case if the food consisted mainly of carbohydrates or meats ; in the case of hyperacidity the pains are generally less severe after abundant meals, even if the latter consisted of foods in themselves difficult of digestion, provided only that they are rich in albumin ; after smaller meals with little albumin the pains are not relieved, for it is the albumin or proteid of the food which alone has binding affinity for the excess of HC1. If the symptoms observed in the patient do not suffice to estab- lish a positive differential diagnosis between ulcer and hyperacidity, it is safer to treat the patient for ulcer — this may be the case when it is impossible to pass the tube on account of suspected ulcer. If the pains become less or cease entirely soon after beginning this treatment, it is probably a case of ulcer, while if they remain the same or increase, it is a case of hyperacidity. If the hyperacidity is removed by this treatment at the same time as the ulcer, this fact suggests that the hyperchylia was not the cause, but the result, of ulcer. On the other hand, if, after curing the ulcer, the hyper- chylia continues, we may presume either an accidental coincidence of the two, or else the hyperacidity has caused the ulcer. In the latter case the breaking out of the ulcer or the formation of new ulcers is to be feared in the future should the hyperacidity continue. Concerning the terminology of this and allied diseases it is necessary to emphasize that the term “ chylia ” refers to the gastric juice as a whole, — i. e ., including HC1, pepsin, and chymosin, — but the word “ acidity,” of course, can not include these ferments. As the HC1 is the principal constituent which is increased, and though the ferments are more active, there is no evidence proving that they are proportionately increased with the acid HC1 in simple hyperacidity or, as it is also called, superacidity — I consider the latter term preferable to the word “ hyperchyliaP Therapeutics. — ( a ) Diet . — The selection of proper diet for these cases is one of the most important duties of the general practi- tioner and specialist. There are two systems of dietetic treatment for hyperacidity. One favors the use of amylaceous diet and the restriction of proteids, because the latter are powerful stimulants to HC1 secretion. The advocates of the other argue that, since the manifold complaints with hyperchylia are a result of the irritation of the nerves of the stomach by free HC1, therefore, in the fixing of a rational diet such foods must be chosen which DIET IN HYPERACIDITY. 829 combine with the greatest quantity of MCI — that is, in the first place, meats ; in the second, vegetables especially rich in proteid. All the stimulants which might further increase the irritation of the nerves of the stomach must be avoided — viz., pungent spices, tapioca, pepper, also mustard, horseradish, ginger, organic acids, such as lactic, acetic, citric, and tartaric acids, fatty acids (rancid fat); table salt must, so far as possible, be kept out of the stomach ; drinks rich in alcohol are injurious — strong beer, heavy wines, but especially whisky and cognac. Food and drink must not be taken too cold (not under 8° to io° R. — io° to 12. 5 0 C.) and not too hot (not over 45 0 R. or 56° C.). After foods in themselves difficult of digestion, the complaints are not increased, provided they contain much albumin, than after easily digestible ones ; nevertheless the latter are to be preferred, and careful preparation is requisite in order to avoid a mechanical irritation of the nerves of secretion. A diet consisting only of carbohydrates is, in our experience, not injurious. I have exhaustively stated the advisability of amy- laceous diet in hyperacidity on pages 195 to 197. Pure fats are allowed in the same quantities as in the case of healthy people. H. Strauss and L. Aldor have given the experimental evidence that fats are digested as well in hyperacidity as in subacidity (“ Zeitschr. f. diat. u. physik. Therap.,” Bd. 1, S. 134). Fats and oils have a tendency to diminish the HC 1 secretion (Pawlow, /. c.) } and therefore have a therapeutic value. As sugar does no harm in the case of most patients, such baked foods (cakes) are to be permitted in which, by a long process of baking or roasting, a part of the starch has been dextrinized : that is, well-toasted bread, cakes, breadcrust soaked in milk, and also certain dextrinized flours (Horlick’s food, Kufeke’s flour, and others).* On account of frequent disturbance of the motility large quantities of water, by which the muscularis of the stomach is unusually distended, must not be introduced at one time; it is much better to give small quantities frequently, by which at the same time the acid contents of the stomach are diluted. Burning thirst is best quenched by frequent imbibing of small quantities of alkaline mineral waters * Since the first edition of this work my experimental results and practical recom- mendations of an amylaceous diet for hyperacidity have been confirmed by Wold Bach- mann (“Archiv f. Verdauungslcrank.,” Bd. v, S. 336), by Chr. Jiirgensen, and J. Justesen (“ Zeitschr. f. diat. u. physikal. Therap.,” Bd. Ill, S. 541) — and the histological observations have been confirmed by H. Strauss and J. S. Myer (“ Virchow’s Archiv,” Bd: cliv). 830 NEUROSES OF SECRETION. (Saratoga Vichy, Geyser, Capon Springs, Apollinaris water, Selt- ers, Geisshubler, Fachinger water), which are rich in alkalies and carbonic acid gas. The latter is not only soothing, but also favors resorption. Since the percentage of albumin of the various foods, and hence also their valence toward HC 1 , vary remarkably, a table of all these foods is given on page 248, showing how much hydrochloric acid they may hold in combination until the appearance of a weak but distinct reaction with the Baeyer-Gunzburg reagent. In the two columns those foods occupy the first places which combine with the least amount of HC 1 ; those which combine with the greatest amount of hydrochloric acid (meat, poultry, game, fish, vegetables, etc.) stand at the end of the column. From this survey it appears that for patients with hyperchylia, veal, beef, mutton, and raw ham (which hold in combination two or three times as much HC1 as the same quantities of sweetbread, liver pudding, and calf’s brain) are to be recommended if the second system on the preceding page is selected. For the same reason the Leube-Rosenthal meat solution, which in itself is easily digestible, can be recommended. Cooked ham and finely minced pork are also suitable meats. Of the other foods, Swiss cheese, Roquefort, pea sausage, brick cheese, and of the various kinds of bread, especially pumpernickel and rye bread are recommended by Fleischer — I have no personal experience with this form of diet. Wheat bread is not so suitable, as 700 gm. of it are necessary to combine with the same quantity of HC 1 , which is held in com- bination by 300 gm. of pumpernickel or 100 gm. of veal. Beer is not suitable. Milk is to be recommended, both on account of its digestibility and composition. If, on account of muscular disturb- ances, it is desired to avoid large quantities of liquids, condensed milk should be advised ; 600 gm. milk, condensed to one-fourth of its volume, combines with as much HC 1 as 100 gm. veal. Cocoa is also to be recommended. If gastric distress and pain appear after supper before bedtime, the patient should drink a cup of lukewarm milk, bouillon with egg, and meat solution, or eat raw ham scraped fine, or one egg, which also combines with a great deal of HC 1 (see p. 248). This large ingestion of proteid and albuminous food, espe- cially advocated by Fleischer for hyperacidity, does not lead to permanent relief, in the author’s experience. According to care- fully conducted experiments and analyses, he is of the opinion MEDICINAL TREATMENT OF HYPERACIDITY. 83 1 that a proteid diet may keep up a hyperacidity because it is a stronger stimulation to HC 1 secretion (see pp. 195-19 7). ( b ) Medicinal Treatment . — We refer to pages 334 to 336 in ex- planation of the use of alkalies in hyperacidity. Magnesia is preferable to the carbonates because it can not form chlorids, which may irritate the mucosa. As may be seen from the table (p. 248), the albuminates of the foods may take up considerable quantities of HC 1 , and after their transformation into peptone hydro- chlorate they aid the nutrition of the body, which is not the case with the chlorids. The digestive products of albumin, hemi- albuminose, and peptone, combine with more HC 1 in the formation of their hydrochlorate compounds than albumin itself (peptone almost twice the amount), and the peptonizing as well as fte decomposition of the peptone hydrochlorate in the blood require some time, so that the HC 1 combined with it does not readily become free again. Some of the alkalies may be taken in the form of alkaline mineral water — Saratoga Vichy, St. Louis Spring (Mich.), Apollinaris, Biliner water, Fachinger, Selters, and French Vichy. Magnesia usta, bicarbonate of soda, sodium biborate (Jaworski, L. Wolff), are best prescribed as indicated on pages 334 to 336. If there is an inclination to the formation of gases, the bicarbonate of soda is to be replaced by magnesia usta in order not to increase the amount of gas by the C 0 2 which is set free from the former. Magnesia usta has also the advantage of forming a chlorid which has a mild aperient effect. The following are the author’s favorite formulae : R. Magnes. ustae, io.o Sodii bicarb., Pulv. rad. rhei, aa 5.0 Ext. belladonnae, . 0.3 M. SiG. — One-half of a teaspoonful three-quarters of an hour after meals. Or— R. Sodii bicarb., Potass, carbonat., Magnes. ustae, aa 5.0 Ext belladonnae, 0*25 Sacchar. lactis, 20.0 M. SiG. — One-half of a teaspoonful one hour after each meal. (See also formulae on p. 338.) Extract of belladonna or atropin has a decided effect in check 832 NEUROSES OF SECRETION. ing the secretion of gastric juice; in some experiments the amount of HC 1 was reduced to one-third or one-half the normal amount (Riegel, “Verhandl. d. Congress, f. innere Medicin,” 1899, S. 328). According to Jaworski’s experiments, the continued use of large quantities of Carlsbad salt and the thermal waters of Carlsbad reduce the secretion of the acids of the stomach ; this might ex- plain the beneficial influence of a protracted stay at Carlsbad (see p. 336). We are assured that the Bedford and the Saratoga Carlsbad mineral waters in our country have an equally beneficial effect. If the pains in the region of the stomach continue in spite of the remedies discussed thus far, narcotics are prescribed, especially ex- trftt of belladonna (0.03 gm. daily) and atropin sulphate (0.0005 to 0.001 gm., or yjTo °f a g ra -i n )> given with advantage, together with magnesia usta or ammoniomagnesium phosphate — substances which not only only have the effect of reducing pain, but also inhibit the secretion of the glands ; codein phosphate (0.03 gm. % to % daily) is a reliable drug for this purpose. Cocain muriate is not suitable on account of the fact that its effect passes away rapidly, but bro- mid of sodium and bromid of ammonium (2.5 to 4.0 in twenty-four hours), when taken for some time, often do good service. Strontium bromid is even better tolerated than the sodium or ammonium salt. On the other hand, the use of morphin muriate must be as lim- ited as possible. According to Hitzig and Alt, morphin muriate is, to a great extent, excreted in the gastric juice and also with the saliva, and therefore reaches the stomach again after absorption. Small quantities of morphin, however, excite the nerves more than they calm them. If the patients complain of severe pains even on an empty stomach (without being able to prove supersecretion or hyperesthe- sia), then lavage of the stomach, irrigation of the mucous membrane, and internal douches, which were first recommended by Malbranc, will give more permanent relief. With very stubborn cramp-like pains in the region of the pylorus (pylorospasm) there is nothing to be done but to remove the strongly acid contents of the stomach with the tube and to wash out the stomach, first with lukewarm water, then with bicarbonate of sodium, and to leave a small part of the latter in the organ. Jaworski’s treatment by stronger or weaker effervescent alkaline waters has proved useful in our experience. The following are the formulae : MEDICINAL TREATMENT OF HYPERACIDITY «33 Alkaline Effervescent Solution. i. II. Strong. Whak. Sodium bicarbonate 8.0 5.0 Sodium salicyl. , . . 2.5 20 Sodium biborat 2.0 1.0 Add above to one liter (one quart) of carbonated water. Directions. — On an empty stomach take x / z of a tumblerful of the stronger solution, No. I, in the morning. After each meal drink ]/ 3 to '/ 2 of a tumblerful of the milder solution, No. II. These solutions are markedly efficacious if the hyperacidity is associated with uric acid diathesis. The electrical treatment has been used successfully by Einhorn for this purpose, and he especially favors the internal galvanization of the stomach. Since the anode has a calming effect upon the irritated nerves (Heidenhain), it is perhaps best to introduce the anode with the intragastric electrode into the stomach filled with moderate quantities of lukewarm water, and to apply the cathode to the sternum, epigastrium, or spine. Constipation will, as a rule, be relieved by neutralization of the excess of HC 1 , but in the rare cases in which it is not, it is to be fought with rhubarb preparations (pulv. rad. rhei, 40.0; natr. sulph., 20.0), Carlsbad Sprudel salts, by injections, massage of the intestines, and glycerin suppositories. Injections of eight ounces of olive oil into the colon, according to Fleiner’s method, is effica- cious in many cases. Since superacidity is frequently a neurosis, we must, in general, influence the nervous system favorably by a sojourn in the country, in the mountains, at the seashore, by cold rubbings, gymnastics, and abstention from severe mental labor. A treatment recommended by Biedert and Langermann (/. c.) has been found serviceable by the author. The stomach is first washed out by a solution of sodium bicarbonate. When the water returns clean, we pour in a one per cent, suspension of magnesia usta ; when this has run out, it is followed by a one-half per cent, solu- tion of tannin. In the place of the latter, particularly when it is not well tolerated, we often use a suspension of bismuth subnitrate ; when the pains are severe, the author prefers lavage, with a suspen- sion of one dram each of bismuth subgallate and bismuth subni- trate in one quart of warm water. 834 NEUROSES OF SECRETION. PERIODICAL ATYPICAL FLOW OF GASTRIC JUICE (Gastroxynsis ( Rossbach ), Gastroxie (. Lepine ), Gastrosuccorrhea Periodica ( Reichmann )). Gastroxynsis, or periodical flow of gastric juice, is an atypical secretion of the peptic glands — atypical because it does not occur after a normal digestive stimulation, but rather when the stomach is empty. The attacks are associated with intense gastric distress, severe spasmodic pain, and vomiting of considerable quantities of very acid gastric juice. This peculiar neurosis is found almost ex- clusively among the educated classes, and particularly among those individuals who are subjected to unremitting mental exertion. In exceptional cases persons belonging to the laboring classes are attacked by it. The malady occurs in attacks which last from one to three days, returning in some instances every week, and in others at intervals of months. The attacks are more frequent when the mental exertion is severest, and become rare as soon as pauses of mental rest intervene. During vacation of these brain- workers, or sojourn at the seashore or in the mountains, the attacks disappear entirely, to return again when the sufferer applies him- self to his profession. The pains, which are most probably caused by irritation of the mucosa, by the intensely acid secretion, are generally preceded by nausea, eructation, and pyrosis. Eventually the emesis of large quantities of acid liquids supervenes, and, as a rule, terminates the attack. The sufferers generally recuperate quickly. Jiirgensen and Ewald have reported cases of typical migraine that were also associated with superacidity. Rossbach (“ Deutsch. Archiv f. klin. Med.,” Bd. xxxv, 1885) and Rosenthal (/. c.) have suggested hypotheses attempting to explain the pathogenesis of periodic flow of gastric juice; their theories are not supported by experimental evidence, and have not cleared up the subject. Etiology. — Among the incidental causes we meet with exces- sive and exhausting mental exertion, intense emotional excitement, anger, nicotin poisoning, and occasionally dietetic errors. The so-called periodic flow of gastric juice, as first described by Reich- mann (“ Berlin, klin. Wochenschr.,” 1882, Nr. 40), and the gas- troxynsis of Rossbach, are, in our opinion, simply phases of the same neurosis, not different diseases. Symptomatology. — The attacks occur very acutely, more fre- quently on an empty stomach, and with a feeling of pressure in SYMPTOMATOLOGY OF GASTROXYNSIS. 835 the head increasing to intense headache, pain in and over the eyes, distress, pressure, and fullness in the stomach, increasing to gas- tralgia. Eructation, pyrosis, and nausea usher in abundant vomit- ing of highly acid mucous masses ; the quantity of HC 1 in the vomit may be fifty per cent, and even exceed this. Repeated vomiting will bring up mucus and bile. When the vomit occurs while the stomach still contains ingesta, this will show the same chemical reactions as are found in hyperacidity. The drinking of water relieves the gastric distress by diluting the acid, but generally in- creases the vomiting. In our experience the attacks occur, as a rule, in the middle of the night, or in the early hours of the morn- ing. The patient has a very pale appearance, and the extremities are frequently cold. A few hours after the first vomiting of gastric juice the attack may be repeated, and again an equally large quan- tity of gastric secretion containing no food particles whatever may be vomited. In a case which the author saw in consultation with Dr. J. B. Schwatka, of Baltimore, the patient vomited surprisingly large quantities of pure straw-colored gastric juice. The amount was between 5 10 and 600 c.c. every time he vomited, which usually was three or four times in twenty-four hours. The patient retained no food for eight days, was fed by nutritive enemata, and finally recovered under lavage with bicarbonate of sodium and spraying the stomach with nitrate of silver 1 : 1000. At night a hypodermic of morphin, gr., and atropin, gr., was given. The acidity of vomit was 3.5 per thousand (free HC 1 ). Occasionally, the gastric pains are the only symptom, and headache follows later on ; in fact, the symptoms might be differentiated into gastric and cerebral symp- toms — at times the former prevail, and at others, the latter. The highly acid liquids in the stomach very likely cause a reflex spas- modic pylorospasm. Eructation, insufficiency of the cardia, and pneumatosis are frequent accompaniments. Periodical atypical flow of gastric juice may be an independent neurosis of secretion, or reflexly caused by diseases of the central nervous system. The gastric crises occurring in tabes have been classed with periodical secretion by some authors, but according to von Noorden (“Charite Annalen,” 1890), Bouveret (/. c., p. 680), and Boas (“ Deutsch. med. Wochenschr.,” 1889, Nr. 42) the liquids vomited in gastric crises are not always acid, and frequently may be found alkaline. They are not associated with the very severe phenomena of highly increased acidity of gastric juice; namely, the strong pyrosis, and the feeling of a corrosive substance in the stomach. Bouveret has NEUROSES OF SECRETION. 836 expressed his doubt concerning the existence of a central form of periodical gastrosuccorrhea. Diagnosis. — Gastroxynsis maybe confounded with the migraine associated with gastric symptoms, with intermittent forms of severe hyperchylia, and with the gastric crises. The diagnosis can be made by chemical analysis of the vomited matter. The attacks usually occur in the midst of good health, and the severe thirst, loss of appetite, cephalalgia, and great prostration are characteristic symptoms. Rossbach found an acidity of four per thousand (HC1) in one of his cases, and Boas found that there was a hyperacidity even in the intervals between the attacks, and that the amount of gastric juice during the attacks was not much increased as com- pared to that found in the intervals. Example I . — Miss M. G., age twenty-four, of neuropathic extraction, has frequently had attacks of vomiting and gastric pain during childhood. For about six years she has suffered from intense pyrosis, which was relieved by bicarbonate of sodium tablets. Sometimes the heartburn ceased after the in- gestion of food. She is a music teacher, and frequently spends eight to ten hours a day teaching pupils and giving singing lessons. The appetite is at all times very good, bowels slightly constipated. The acidity after our double test-meal taken in the interval between the attacks is equal to 0.3 per cent. HC 1 . About once a week she has distressing attacks of gastralgia, associated with severe headache and vomiting of very acid liquid masses. The attacks occur generally between two and three o’clock in the morning, when she has spent a day at hard work teaching pupils. The patient awakes suddenly with a feel- ing extending from her stomach to her throat, which is described as a twisting of the gullet. Severe cephalalgia, giddiness, nausea, and vomiting follow. Sometimes she does not vomit, but the attack is passed off by rapidly drinking a half-pint of water with a teaspoonful of bicarbonate of soda. Physical ex- amination, entirely negative. Urine, the indican is increased. Urea, uric acid, ratio high. No splashing sound in the stomach prior to ingestion of food or drink. Acidity of filtrate of vomited matter, which apparently was free from bile, was equal to 2.8 per thousand (HC 1 ), or 0.28 per cent. The fact that the acidity was less during the attack than during the intervals, suggested that the HC 1 had been neutralized through bile, duodenal secretions, or saliva, but the care- ful examination for these constituents was negative. During a summer vaca- tion in which the patient undertook a trip to Europe, she vomited daily from sea-sickness, but in three months, while she was in Germany, she did not have one attack. On returning, the acidity, after a similar test-meal, as before stated, was equal to 1.5 per thousand (HC 1 ). General condition much improved. Example II . — This case is that of a colleague, a friend of the author’s, who has described his case with great accuracy on repeated occasions. The attacks usually occur at night, associated with headache and gastric distress, and cul- minate in the vomiting of large masses of highly acid material. The doctor is an indefatigable brain-worker, allowed himself very little, if any, recreation. CHRONIC SUPERSECRETION. 837 His general nutrition is good, and he has found that his attacks are rapidly relieved by the taking of ordinary cane-sugar (Ewald). Periodical vomiting, when associated with hyperacidity, must be carefully distinguished from gastroxynsis. Treatment. — This includes, in the first place, the avoidance of stimulants and narcotics: alcohol and tobacco, as well as strong coffee. It is most essential that the patients should avoid mental overwork. They should, in fact, refrain from brain-work altogether, and allow themselves three or four months a year to enjoy recreation in the mountains or at the seashore. Physical exercise should be indulged in moderately but systematically. The bicycle is an excellent remedy for periodical flow of gastric juice; and also horseback riding, swimming, rowing, fencing, gymnastic exercises, and outdoor games. During the attack itself, the effects of the excess of acid should be counterbalanced by copious drafts of suspensions of calcined magnesia, ammonio- magnesium phosphate, or bicarbonate of sodium. When the vomiting has occurred at short intervals, one should not hesitate to pass the stomach-tube, wash out the stomach with sodium bi- carbonate, and afterward treat the mucosa with suspensions of bis- muth subgallate (Sij to Oj) or with argentic nitrate, I : 1000. A mustard plaster should be placed over the epigastrium. If this can not be conveniently had, a hot-water bag will act similarly. The bromid of strontium and bromid of ammonium, in doses of thirty grains three times a day, have an undeniable effect upon the frequency of the attacks. The diet should be carefully adjusted to the digestive capacity of the stomach. We usually recommend Penzoldt’s diet order, which is given among the diet lists. In the intervals between the attacks the patients should undergo treat- ment as outlined for hyperacidity. Belladonna or atropia are often valuable aids to the treatment; their mode of action has been explained on page 830. CHRONIC CONTINUOUS FLOW OF GASTRIC JUICE (Chronic Hyper- or Supersecretion (Riege/), Gastrosuccorrhea Chronica ( Reichmann ). We have our doubts whether such a condition of permanent irritation of the gastric secretory nerves and uninterrupted secre- tion exists as a primary disorder. Chronic gastrosuccorrhea, which 55 8 3 8 NEUROSES OF SECRETION. Reichmann claimed to have observed and first described in 1882 (‘‘Berlin, klin. Wochenschr.,” 1882, Nr. 40; 1884, Nr. 48; 1887, Nr. 12) as a disease peculiar to itself, is stated by him to be a dis- order characterized by the chronic uninterrupted secretion of gastric juice at all times, even when there is no food in the stomach. In a fasting condition in the morning, Reichmann and others claim that gastric juice could be drawn from the stomach in these cases. As we have seen in the description of the organic gastric diseases, particularly in severe reflex neuroses, in dilation, and gastric ulcer, continued flow of gastric juice is a frequent symptom, asso- ciating itself with alteration and loss of substance in the mucosa. Occurring as a secondary affection, it may still be able to effect severe damage to the gastric walls. The diagnosis of this hypo- thetical disease hinges upon the presence of gastric juice contain- ing HC 1 and ferments in the jejune or fasting stomach. This question has been very carefully investigated by Schreiber (“ Deutsch. Archiv f. klin. Medizin,” Bd. liii, S. 90). He found, in Konigsberg, that in over 70 per cent, of his patients a digestive secretion was contained in the fasting stomach. Physiologically speaking, an absolutely clean and empty stomach should, in the morning, contain no gastric juice, as the glandular apparatus is normally in a resting state, but practically the human stomach is very rarely in this condition. It contains at all times epithelial detritus, dust, bacteria, secretions from the mouth, lar- ynx, and pharynx, particularly saliva, which at different intervals are swallowed consciously or unconsciously. These albumin- ous, mucous masses, which are generally weakly alkaline, and which collect particularly during the night, incite the specific gas- tric glands to secrete their physiological product just as any weakly albuminous food would do. This is a kind of pseudo or frustrate digestion, because, so far as nutrition is concerned, this slow digestion going on constantly is of no value. This slight pseudodigestion, which, according to Schreiber, is present perhaps at all times, is augmented and multiplied by the permanent pres- ence of actual food masses when the stomach is dilated. The frustrate digestion becomes a real one. In all dilations with reten- tion of food we have a permanent, real digestion, and an augmented permanent secretion corresponding to it. This so-called continued hypersecretion leads to the digestion and assimilation of proteids and albuminous bodies of the food, while the normal digestion of carbohydrates is impeded. The NATURE OK SUPERS ECKETION. 839 phenomena that are claimed to be typical of chronic continued hypersecretion are unavoidable consequences of dilation. The cardinal point of distinction — namely, that digestive secretions are contained in the stomach on the morning following a very effective washing out executed the evening before — is certainly not peculiar to chronic hypersecretion, but occurs also with dilation. Schreiber has called attention to the fact that it is exceedingly difficult, even impossible, to completely evacuate and clean out a dilated stomach. During gastrotomies food substances have been found in the stomach, notwithstanding very energetic efforts to free it of all remnants beforehand. When a patient with a dilated stomach is to be examined for the gastric contents prior to taking food in the morning, it is expedient not to be satisfied with the simple expres- sion method of Ewald, when this is negative, but to place the patient in a horizontal position, and, while he makes efforts at straining as if he were bearing down for stool, the operator must compress the stomach near the fundus, which, in these cases, is sometimes found below the umbilicus. In the reports of a number of advocates of chronic hypersecre- tion as a primary disease per se , one frequently finds that the authors state that small quantities of food remnants were found in the fasting stomach. The argument generally follows that such small quantities of food could not be the cause of the large quantity of gastric juice secreted, contending that the latter must have been secreted spontaneously. At the same time, an illogical position is demonstrated by the assertion that the momentary contact of a soft stomach-tube with the mucosa is the cause of the secretion of eighty to one hundred centimeters of gastric juice. This assertion, it should not be forgotten, is made by a number of those who have found food remnants in the stomachs of these cases. That is to say, the effort is made to ignore the physiological stimulus of food which is contained in the stomach for hours, and emphasize the rather insignificant momentary stimulation caused by the introduction of a tube. As Schreiber correctly points out, the freedom of the stomach contents from food particles is very often only an apparent, not a real, one. It is caused by imperfections in our methods of investigation, and when one closely considers the symptoms of chronic hypersecretion, as they are described by the adherents of Reichmann, they seem, in many cases, to be identical with those of dilation. We have been able to exclude the hypo- thetical factor of the stomach-tube in causing a secretion of gastric 840 NEUROSES OF SECRETION. juice in a normal fasting stomach. In a number of our students who consented to take a hypodermic injection of apomorphin before they had eaten anything in the morning, we demonstrated the presence of HC 1 in the vomited matter. There is, therefore, in some persons and to some degree a physiological normal continued secretion of gastric juice, as Schreiber correctly asserts (“ Deutsch. medizin. Wochenschr.,” 1894, Nr. 18-21); in these the stomach secretes gastric juice normally and independently of the ingestion of food. Ewald and Boas cite a case which has been quoted by Riegel (“Deutsch. med. Wochenschr.,” 1893, Nr. 31, 32) in oppo- sition to the views of Schreiber. This female patient had a pecu- liar gastric neurosis founded on a hysterical basis. For six years the patient vomited everything that was ingested ; fluids were vomited immediately, and solid food after two to four hours. When she had taken 100 c.c. of water on an empty stomach in the morn- ing, she vomited it very soon thereafter, and Ewald and Boas could not find free HCl in it, and therefore concluded that the fasting stomach secretes no gastric juice under normal conditions. Aside from the fact that this woman may have had a spasm of the esophagus or cardia preventing the small amount of water from ever reaching the stomach, it is not fair to decide a physiological question from results obtained from a chronic neurotic patient ; for, as we know, in this class of individuals the greatest variation in the state of the gastric secretion exists (see Heterochylia). The results obtained on human beings with gastric fistulae (see W. Beau- mont on his Canadian hunter, Alexis St. Martin, also the cases of Kretschy-Richet) are inadmissible to the solution of this physio- logical question, because they are made on individuals under patho- logical conditions. The existence of HCl in normal stomachs may be demon- strated by giving healthy individuals long pieces of thin thread, which with some practice they can learn to swallow on an empty stomach ; this silk or thread is so thin that it does not irritate the gastric wall to any degree, at least not so much as a stomach-tube ; the thread is then rapidly withdrawn and pressed between pieces of Congo paper, when it can be seen that the Congo paper turns dark blue. We have also introduced the thread already stained with Congo red, and obtained the blue discoloration from fasting normal stomachs. Undoubtedly there are great individual varia- tions in the genuine as well as in the frustrate digestion, caused by the secretive power of the glands and the character of the food. TYPES OF CHRONIC GASTKOSUCCOfcKHKA. 84 I Morbid conditions influence both of these types of digestion quantitatively and qualitatively. Conditions which incite the glands will increase the HC 1 , and conditions which weaken the mucosa, such as gastritis, diminish the HC 1 during real digestion after meals, as well as during the frustrate digestion occurring during the night and on a fasting stomach. These variations are also frequently found in dilation. If the gastrectasia occurred on the basis of an ulcer, the true secretion, as well as the permanent secre- tion of a frustrate character, will be increased, and reversely, when carcinoma or chronic gastritis is present, together with dilation, both kinds of secretion will be diminished, or they may not contain HCl at all. In diagnosing a dilated stomach it is important to bear in mind that a stomach may be very much enlarged and still its greater curvature may not have descended to any considerable extent. Frequently the very cause that has brought about dila- tion — for instance, perigastritis, or adhesions about the stomach — makes a descent of the greater curvature impossible, simply because it can not descend, being bound down into this position in the upper part of the abdomen by inflammatory adhesions. Therefore it is possible that a stomach may be dilated and yet give no splashing sound about the neighborhood of the umbilicus, nor need it be much displaced from its normal position. The stomach may, in fact, enlarge in an upward and backward or lateral direction when its descent is made impossible by adhesions. The presence or absence of food particles in contents drawn from the fasting stomach can not always be recognized by the naked eye. What resembles a turbid liquid free from ingesta to the naked eye, will often show undigested rice, bread, and other carbohydrates under the microscope. There is, however, a second class of cases of chronic continuous flow of gastric juice in which absolutely no organic disease of the stomach and no dilation are demonstrable. These are the typical cases of Reichmann and Riegel, and due to exces- sive reaction of the gastric mucosa to the stimulation of the ingesta. We have personally seen cases which, according to the description of Reichmann and Riegel, would have to be classed as typical chronic hypersecretion, in which the stomach was appar- ently in its normal place, and no organic gastric disease could be determined with the most exact methods of examination. In three of these cases we could extract from 100 to 150 c.c. of gastric juice from the fasting stomach, apparently containing no food con- tents but occasionally containing traces of bile. The acidity of 842 NEUROSES OF SECRETION. this secretion when filtered was equal to 8o° HC 1 by decinormal solution of sodium hydroxid and either Congo or dimethylamido- benzol. The total acidity was no in one of the cases- — that of a young bank clerk twenty-four years of age. He also suffered from con- stipation, pyrosis, increasing to pain, and vomiting which came on very soon after meals. The examination of the contents one hour after our complex test-meal gave the following results: Total acidity, 108 ; free HC 1 , 84; biuret reaction, positive ; patellar and pupillary reflexes, normal. For eight consecutive days free HC 1 and gastric ferments could be detected in the contents from the fasting stomach. As his trouble was persistent and he was deter- mined to get well, he consented to a course of exclusive rectal feeding. He was nourished for ten days by the rectum, and at the same time his stomach was washed out with suspensions of magnesia usta every day. Under these conditions, when no food was ingested per os, the gastrosuccorrhea rapidly diminished, and disappeared entirely on the fourth day, so that not even the swallowed masses of mucus and saliva could sufficiently stimulate the mucosa to pro- duce a secretion of HC 1 . This has occurred in three of our cases where the amounts of gastric juice found on an empty stomach exceeded 100 c.c. A second one of these cases was that of a young girl with chronic flow of gastric juice, who was operated on upon our suggestion by Dr. R. W. Johnson at the Maryland General Hospital. After the abdomen was opened and the stomach incised, no anatomical cause for the persistent vomiting and gas- tralgia could be detected. On replacing the stomach, however, and inserting the finger into the pylorus, a rather sharp bend in the duodenum was evident to the author. Undoubtedly this kink became more manifest when food was ingested, the stomach thereby dragging upon this acute angle in the duodenum. It was one of those cases of motor insufficiency which Broadbent has described (“British Medical Jour.,” vol. 11, 1893, pp. 1193 and 1268) due to kinking of the duodenum by an abnormally short duodenohepatic ligament. During the operation the pylorus was also enlarged by sewing together the oblique incision which had been made (it is true only for explorative reasons), but was in closing up sutured in such a way as to resemble a pyloroplastic operation. The patient made a perfect recovery, and there was no more gastrosuccorrhea, vomiting, or gastralgia. She remained in the hospital for two months after the operation, CONCLUSIONS REGARDING CHRONIC HYPERSECRETION. 843 and was not supplied with specially prepared diet, but lived upon the regular hospital fare without gastric distress, and was dis- charged in good condition. Einhorn (/. c. f p. 313) agrees with Reichmann as to the existence of a pathological continuous gas- trosuccorrhea, although he restricts this name to cases not present- ing organic lesions of the stomach. Whenever the latter exists (lesions), he looks upon the accompanying gastrosuccorrhea as a consequence of the main trouble, but not as a cause of the organic lesion. It is the exclusion of these organic troubles, particularly of enlargements of the stomach and motor insufficiency, in which the greater curvature has not descended, which presents so much difficulty. In all* the cases of chronic continued hypersecretion that we have examined with regard to this question, we were enabled to discover some organic lesion, most frequently an atony, pyloric stenosis, or dilation from some cause. After a careful in- vestigation of a large clinical material I incline to the opinion that chronic hypersecretion is in the majority of cases not a sponta- neous, idiopathic neurosis, but a secondary symptomatic phenom- enon. I base my conclusion upon the following facts : (1) That gastric juice in amounts varying between 20 and 30 c.c. is con- tained normally in the fasting stomach in about 8 per cent, of cases examined by myself; the secretion of the peptic glands being set up by the presence of mucus, saliva, dust, bacteria, epithelial detritus, etc. (2) That apparently clear gastric juice obtained from a fasting stomach may show presence of food par- ticles microscopically. (3) That it is not possible to exclude dilation nor ulcer in all of these cases, particularly when the dila- tion is not marked by the descent of the greater curvature. (4) The liquid obtained from undoubted dilations of the stomach may contain absolutely no food particles, thus simulating the condition for chronic gastrosuccorrhea. (5) Gastric contents obtained from dilation of the stomach do not always show the presence of products of imperfect starch digestion (erythrodextrin). This is particularly the case when we meet with dilation accompanied by hyperacidity, but with a fair motility, or where the peristalsis is only periodically lost. In any case of hyperacidity it is possible that the products of starch digestion may be absent when very little carbohydrate food has been ingested. This may, of course, also happen with gastrosuccorrhea. (6) In cases of typical, so-called chronic, continued supersecretion, the symptoms cease entirely and the stomach contains no gastric juice in the morning after the 844 NEUROSES OF SECRETION. patient has been fed by the rectum for four to eight days. (7) Diseases presenting the classical picture of Reichmann’s disease have been known to disappear entirely after a gastro- enterostomy or a pyloroplastic operation was performed. Symptomatology. — This is essentially the same as in motor insufficiency with hyperacidity. (See chapter on this subject.) The periodic flow of gastric juice, which we have already described (p. 834), is either a functional neurosis or a reflex affec- tion (tabes dorsalis), or connected with an affection of the sym- pathetic. It is identical with the gastroxynsis of Rossbach. Possibly, also, the periodic vomiting of Leyden belongs to this group of neuroses. The chronic gastrosuccorrhea is a symptom , and has not the claim to be considered a morbid entity like the periodic or spasmodic gastrosuccorrhea. Chronic flow of gastric juice may be a complication of ulcer and motor insufficiency. From a pathological standpoint, it is well established that gastritis may accompany ulcer as well as dilation (Rokitansky, Lebert, Orth, Cruveilhier). The gastritis which accompanies these dis- eases, and which shows hyperacidity, has been called by Kor- czynski and Jaworski (“ Deutsch. Archiv f. klin. Med.,” Bd. xlvij, S. 578) “ catarrhus acidus,” and by Hayem (“Gazette Hebdom.,” 1892, Nos. 33 and 34) it has been designated as “ gastrite hyper- peptique.” These expressions signify the same complexity of symptoms as those first described by Reichmann under the name of “ gastrosuccorrhea.” The “ gastritis acida ” of Boas is quite a different thing — a characteristic form of chronic gastritis. Diagnosis. — The main question to decide is not whether we are dealing with chronic gastrosuccorrhea, which is not very difficult to find out, but to determine which disease it is a con- sequence of. The most frequent causes are ulcer, pylorospasm, and mechanical insufficiency. For a fuller explication of these subjects and their consequences we must refer to the chapters in which they are considered. If 150 to 300 c.c. of gastric juice can be drawn from the stomach before taking food in the morn- ing, which juice is free from food remnants, and there are no evidences of motor insufficiency, the case will be one of primary neurotic chronic gastrosuccorrhea. But if the food remnants are very evident and especially if organic diseases are demonstrable, the condition is secondary. Treatment. — If ulcer, pylorospasm, or dilation can be demon- strated to exist, the treatment must be directed to these fundamental LITERATURE ON CHRONIC GASTROSUCCORRHEA. 845 causes. (See Treatment of Ulcer and Motor Insufficiency.) In the absence of any definite etiological factor, the treatment is that de- scribed under hyperchylia. Under all conditions massage of the stomach and intestines, intragastric application of the galvanic and faradic currents, and washing out of the stomach are very essential adjuncts to treatment. Where there is much secretion of gastric juice, even on an empty stomach, the use of a stomach-tube can not be consistently neglected. It is the only way to remove the excess of secretion directly; then, again, the best treatment of a hyper- chylia is that which is supplied directly to the mucosa in the form of irrigations with calcined magnesia, sodium bicarbonate, tannin ( ]/ 2 of one per cent, solution), and suspensions of bismuth subnitrate. The methodical use of alkalies affords great relief to the pyrosis and eructation, and facilitates carbohydrate digestion. The alka- lies which we recommend most strongly are the magnesia usta and the ammoniophosphate of magnesium. Einhorn speaks very favorably of spraying the stomach with a solution of nitrate of silver, I : 1000. Reichmann administers the nitrate of silver in solution or in gelatin capsules. The author uses this salt in the form of lavage (i : 1000) and can speak with favor of this treatment. The diet will vary with the underlying causative disease. It will be either that for ulcer or dilation, or that for hyperchylia. Where the stomach is extremely sensitive, the diet orders of Penzoldt may be safely tried, because they are very sparing and make little de- mands upon the capacity of the stomach. Exclusive rectal feeding may be necessary ; it is, as a rule, promptly followed by good results. Dr. D. L. Edsall has given a lucid representation of recent litera- ture on this subject (“ Amer. Jour. Med. Sciences,” vol. cxvii, 1899, p. 694). LITERATURE ON CHRONIC GASTROSUCCORRHEA. 1. Boas, “ Specielle Diagnostik u. Therapie d. Magenkrankheiten,” 2. Aufl. 2. Bouveret et Devic, “ La Dyspepsie par Hypersecretion Gastrique ” (Mala- die de Reichmann), Paris, 1892. (Monograph.) 3. Cavazzani, A., “ Della malattia di Reichmann e della sua cura,” “ Clin. Med. Ital.,” Milan, 1898, xxxvn. 4. Combemale, “Maladie de Reichmann un Dyspepsie par Hypersecretion Gastrique,” “ Echo Med. du Nord,” Lille, 1897, 1. 5. Debove et Remond, “ Les Maladies de l’Estomac.” 846 NEUROSES OF SECRETION. 6. Faucher, “ De la Crise Aigue dans la Maladie de Reichmann” (Gastrite Chronique avec Hypersecretion), “Jour, de Med. Prat.,” 25, vi, 1897. 7. Hayem, “ Resume de l’Anatomie Pathologique de la Gastrite Chronique,” “ Gaz. Hebdom.,” 1892, Nos. 33, 34. 8. Hayem, “ Ueber Gastritis parenchymatosa,” “Allgem. Wien. med. Zeitung,” 1894, No. 2 ff. 9. Hayem, “ Stenose incomplete du Pylore, Pretendue Maladie de Reich- mann,” “ Presse Medicale,” 31 mars, 1897. 10. Jaworski, “ Zeitschr. f. klin. Med.,” Bd. XI, Heft 2 u. 3 ; “ Munch, med. Wochenschr.,” 1887, No. 7 u. 8 ; “Wien. med. Presse,” 1886, No. 52; “Wien, med. Wochenschr.,” 1887, No. 49 u. f. 11. Johnson, E. E., “ Munch, med. Wochenschr.,” 1887, No. 48 u. f. 12. Johnson und Behm (“Zeitschr. f. klin. Med.,” Bd. xxn, S. 478), “Re- port of 106 Cases of Supersecretion,” including all cases where slight amounts of gastric juice were found, and give complete literature. 13. v. Korczynski und Jaworski, “ Deutsches Archiv f. klin. Med.,” Bd. XLVII, S. 578. 14. Leyden, “ Zeitschr. f. klin. Med.,” 1882, Bd. vi, S. 605. 15. Linossier, “ Maladie de Reichmann et Stenose Pylorique,” “ Semaine Med.,” Paris, 1898, xvm. 16. Lyon, G., “ L’ Analyse du sue Gastrique,” Paris, 1890. 17. Lyon, G., “ Les Theories Nouvelles sur la Gastrosuccorrhee ou Maladie de Reichmann et sou Traitement,” “ Rev. de Therap. Med. et Chir.,” Paris, 1897, LXIV. 18. Martius, F., “ Ueber den Inhalt des gesunden, niichternen Magens und den continuirlichen Magensaftfluss,” “Deutsche med. Wochenschr.,” 1894, Nr. 32. 19. Morano, G., “ Malattia di Reichmann,” “ Riforma Med.,” Napoli, 1898, xiv, pt. 4. 20. Reichmann, “ Berl. klin. Wochenschr.,” 1892, Nr. 40; 1884, Nr. 48; 1887, Nr. 12 u. f. ; 1887, Nr. 14. 21. Riegel, “Zeitschr. f. klin. Med.,” Bd. xi u. XII ; “ Munch, med. Woch- enschr.,” 1884, Nr. 45 u. 46; “Deutsche med. Wochenschr.,” 1887, Nr. 29; 1892, No. 21 ; 1893, Nr. 30 u. 31 ; “ Volkmann’s Samml. klin. Vortrage,” 1886, S. 289. 22. Rosin, “ Ueber das Secret des niichternen Magens,” Deutsche med. Wochenschr.,” 1893, Nr. 30. 23. Rossbach, “ Deutsches Archiv f. klin. Med.,” 1885, Bd. xxxv. 24. Roux, “Le Syndrome de Reichmann, Expose Critique des Travaux Recents sur l’Hypersecretion Chlorhydrique Continue,” “ Gaz. des Hopit.,” No. 61, 1897. 25. Saupault, “ Sur Un cas de Gastro-succorree,” “ Gaz. Hebd. de Paris,” 27 Janvier, 1897. 26. Schreiber, Jul., “ Gastrektasie u. deren Verhaltniss z. chronischen Hyper- secretion,” “Archiv f. Verdauungskrankh.,” Bd. 11, S. 423. 27. Schreiber, Jul., “Ueber den continuirlichen Magensaftfluss” (Secretio hydrochlorica continua), “ Deutsche med. Wochenschr.,” 1893, Nr. 29 u. 30; ibid , “ Ueber continuirlichen Magensaftfluss,” “ Deutsche med. Wochenschr.,” 1894, Nr. 18, 20, u. 21. SUBACIDITY. 847 28. Sticker, “ Munch, med. Wochenschr.,” 1886, Nr. 32 u. 33. 29. Strubing, “Zeitschr. f. klin. Med.,” 1885, Bd. ix, S. 381. 30. Vente, A., Inaug.-Dissert., Giessen, 1890. 31. Wolff, “Zeitschr. f. klin. Med.,” Bd. xvi. 32. Text-books of Leube, Riegel, Boas, Ewald, Debove et Rdmond, Bou- veret, Penzoldt, Fleiner, S. Martin, A. Pick, Mathieu, Einhorn. 33. Edsall, D. L., “ Amer. Jour. Med. Sciences,” vol. cxvii, 1899, p. 695. SUBACIDITY (Hypochlorhydria or Hypochylia). Subacidity, as a neurosis, is a disease in which, even during the height of digestion, gastric juice is secreted in which the HC1, and with it the pepsin and rennin, are present in smaller amounts than normal. We will not consider under this head those secretory anomalies in which the secretion of gastric juice is absent entirely. These states will be considered under Achylia Gastrica or In- acidity. In subacidity HC1 is still secreted, but in such small amounts that it enters into combination with albuminous foods entirely, and we can detect it only as combined HC1. Cases in which free HC1 can be detected by Congo paper after our double test-meal do not logically belong in this class of subacidity, because the presence of free HC1 means that more HC1 is secreted than can enter into combination with the food ; there is an excess of acid beyond that required for digestion. Technically, we may, therefore, define hypochylia as a secretory neurosis in which free HC1 is absent at the test-meal, but combined HC1 and the ferments are still present. Nervous hypochylia is in reality but a phase of nervous dyspepsia, or neurasthenia gastrica. But, as it is desir- able to represent all secretory neuroses seriatim, we have here abstracted the symptoms of nervous depression of gastric secre- tion. It was formerly believed that subacidity was always con- nected with some organic gastric disease (carcinoma, gastritis), or occurred in the train of infectious diseases, or, as a result, with anemia and leukemia. Subacidity, however, may exist on a purely nervous substratum, in hysteria and neurasthenia, and in psychoses. It then occurs, independently of anatomical changes in the stomach, as a functional disturbance of the secretory nerves, the irritability of which has been reduced. Functional disturbances of this char- acter may be limited to the secretory nerves and not involve the remaining nervous apparatus of the stomach. The amount of HC1 secreted is not sufficient to saturate the albumin present in the proteid food : in other words, an HC1 deficit exists. It is probable 848 NEUROSES OF SECRETION. that the secretory nerves become exhausted sooner than the motor nerves, and that, therefore, subacidity may be an expression of ex- haustion or weakness in the secretory apparatus. In this way we have repeatedly observed prolonged subacidity followed by pro- nounced hyperacidity. Etiology. — Nervous subacidity or hypochylia is a secondary phenomenon occurring with neurasthenia, hysteria, tabes, and the psychoses. Symptomatology. — When the motor function of the stomach is good, symptoms may be absent entirely, but the slightest insuffi- ciency of the motor power is rapidly followed by decomposition in the gastric contents, caused by bacteria, for the amount of HC1 secreted is not sufficient to inhibit or prevent the action of micro- organisms. As a consequence of this organic acids are formed, and gaseous formations create gastric discomfort, and, at times, intestinal distention. There is nothing characteristic in the symp- tomatology of subacidity. The result of the depressed state of the secretion and the general symptomatology are the same as those in achylia gastrica, and will be described under that heading. It is natural that amylolysis should proceed more rapidly in the absence of free HC1, since nothing can disturb the activity of the ptyalin in that case. On the other hand, the digestion of meats, eggs, etc., is most unsatisfactory. As HC1 is one of the principal normal stimulants to peristalsis, the disease is frequently accom- panied by constipation, which, in turn, produces increasing putre- faction of the intestinal contents, being in this case more pro- nounced because the disinfecting action of the HC1 is missing. Differential Diagnosis. — Carcinoma and chronic gastritis might be confounded in the incipient stages with nervous subacidity (for the differential diagnosis from carcinoma and gastritis, we refer to the chapters on these diseases) ; but when the enzymes, pepsin and rennin, can be demonstrated in the gastric contents, or even if only the proenzymes, pepsinogen and rennin-zymogen, can be demonstrated, one can not, as a rule, exclude chronic gastritis and carcinoma. A patient and prolonged study of nervous sub- acidity will not fail to demonstrate that great variations exist in the amount of hydrochloric acid that is secreted. Occasionally it may be found that a transition to a normal acidity, or even to hyper- chylia, has taken place. Lactic acid is a very rare occurrence in nervous subacidity; its presence and the Oppler-Boas bacillus would speak for carcinoma. TREATMENT AND DIET IN SUBACIDITY. 849 Treatment. — In most cases it will be sufficient to supply an amount of dilute HC1 which is commensurate with the deficit. In rare instances it will be impossible to administer sufficient HC1 to give the reaction for free IIC1, because it is not well tolerated in this quantity. In that case we advise adding the HC1 to beef- juice, either Wyeth’s, Valentine’s, or the Mosquera beef-jelly. This makes a sauce which can be poured over the finely divided meat foods that are to be eaten. The meat-dissolving power of the acid is not destroyed by this method of preparing it, although the acid may be partly in a combined state. Abnormal fermentations and decompositions are rare, and therefore the stomach-tube can, as a rule, be dispensed with. The bitter tonics — quassia, cinchona, calumbo, gentian — and the basic orexin (in five-grain doses three times a day) very often increase the appetite and favor a secretion of HC1. Strychnin and the intragastric use of the faradic current we warmly recommend for this purpose. Pilocarpin, according to Riegel, increases the secretion of gastric juice, but in my experi- ence it is too dangerous a drug to use with that persistence that is requisite in these cases. When the motility is good, those mineral waters which are rich in sodium chlorid are worth a trial. (See section on Mineral Waters.) The Diet. — It is an interesting fact that patients with sub- acidity instinctively avoid a meat diet, and are large carbohydrate eaters. It is well, however, not to let them persist on the exclusive use of carbohydrates, but to train up the digestive capacity of the stomach to a more abundant digestion of proteids. All meats should be given in a finely divided state. The extractive materials in meat are useful stimulants to appetite (Pawlow). Before the meal, it is well to stimulate the appetite and secretion by giving a few sardels or the roe of potted herring, or, what is more palat- able and easier to procure, a sandwich spread with Russian caviar. Surf-baths, cold sponge-baths at home, proper movements of the bowels, and at least eight to nine hours of sleep, are indispensable agents in the management of this secretory defect. 850 ACHYLIA GASTRICA. CHAPTER XIII. ACHYLIA GASTRICA. Synonyms . — Absence of the Secretion of Gastric Juice; Nervous Inacidity; Atrophy of the Stomach; Anadenia Ventriculi ; Phthisis Ventriculi ; Achlor- hydria. Nature and Concept. — The term achylia gastrica means, liter- ally, without gastric chyle, and was first proposed by Einhorn (“ New York Medical Record,” June 11, 1892) to designate a class of diseases in which no gastric juice is secreted. The affection is found to exist in two varieties — first, the pri- mary, idiopathic, possibly inherited, achylia; secondly, the acquired or secondary achylia. The primary idiopathic or symptomatic achylia is characterized by the fact that absence of secretion is evident before any marked anatomical changes have occurred in the mucosa which could explain the loss of function. It is, there- fore, as a rule, not regarded as a result acquired from a real disease, but as an individual peculiarity, possibly an inherited functional debility. There are undoubtedly persons in whom gastric secretion may be absent for years, or permanently wanting; yet who, apparently, may enjoy robust health. The majority of these individuals, however, have suffered from frequent dyspeptic complaints, which are partly of a purely nervous character. In these cases severe anemic and cachectic conditions are usually absent, and while the general nutrition may occasionally be found disturbed, it is easily remedied with proper dietetic treatment. The last-named type of cases demonstrates that the function of the stomach may be permanently lost, so far as its digestive power is concerned, yet with no apparent effects upon the general con- stitution. A very convincing argument for the compensatory digestive power of the intestine! Lubarsch (“ Achylia Gastrica,” etc., von Martius u. Lubarsch, 1897, p. 74) raises the question whether gastric digestion may not be entirely dispensed with, or whether it is not superfluous, which of course implies that the secretion of HC 1 may possibly be an unnecessary function. There can be no doubt, however, that deficiency of gastric secretion is a disease. Individuals affected with symptomatic achylia are very much more sensitive in general, and more susceptible to gastric NATURE OF ACHYLIA. 85 diseases, than their fellow-men equipped with normal stomachs. The idea that gastric digestion is superfluous and dispensable im- presses us as being a reactive opinion induced by the other extreme view formerly held, according to which the stomach was the most important of all digestive organs. Gastric secretion is by no means a useless function. Lubarsch says: “Those who have lost it, have one weapon less in the struggle for existence,” and clinical experience teaches that persons who have no secretion of gastric juice are much more liable to diseases of the stomach. When such are attacked by intestinal diseases and this supple- mentary digestion is interfered with, the prognosis becomes serious. Achylia may exist upon a nervous basis, it may be congenital or acquired, in consequence of some organic gastric disease. The results of the examination of the gastric contents, in simple, uncomplicated achylia, are quite characteristic : The fasting stom- ach, examined in the morning before any food has been taken, is empty. I have never been able to obtain more than twenty to thirty cubic centimeters of neutral, slightly mucoid liquid; remnants of ingesta of the previous day are never observed. One hour after the Ewald test-breakfast the contents of the stomach have the same appearance as they have in the mouth before they are swallowed. This appearance is claimed by Einhorn and others to be quite characteristic. Contents drawn in this manner are generally slightly acid. Blue litmus paper is very slightly red- dened. The total acidity varied in our cases from two to eight. This degree of acidity can be found in the test-meal before it is eaten. Whenever the acidity of the drawn stomach-contents does not exceed that of the meal before it is swallowed, it may be safely assumed that free and combined HC1 is absent; in other words, no HC1 has been secreted. Whenever the total acidity is equal to four only, it is due to acid that has been introduced in the food; with a total acidity no higher than four, one hour after a test- breakfast, it is, therefore, unnecessary to make further analyses for the detection of HC1. The gastric contents, when filtered and mixed with HC1 sufficient to produce the reaction with Congo paper, can not digest discs of egg-albumen. Milk taken by achylic patients may be drawn out twenty or thirty minutes afterward perfectly unchanged, or, rather, uncoagulated. The secretion of pepsin and rennin is, therefore, absent. By proper tests it can also be found that pepsinogen and rennin- 852 ACHYLIA GASTRICA. zymogen are also wanting. Lubarsch and Martius assert that the isolated loss of HC 1 , without loss of secretion of pepsin and ren- nin, does not exist ; and for these cases of loss of gastric secre- tion (not the HC 1 simply, but all the constituents of gastric juice) the terms anacidity, inacidity, and achlorhydria are not so expres- sive and logical as the designation “ achylia gastrica.” We may assert, however, on a very large personal experience, that isolated loss of HC1 secretion and preservation of formation of ferments does occur. In the progressive destruction of the mucosa accom- panying carcinoma and gastritis there are stages in which HClis totally wanting, and yet, by proper methods, secretion of enzymes, or of the proenzymes, can be detected. All other cases of loss of secretion not due to carcinoma or atrophic gastritis may logically be classed as achylia. A further pronounced sign of achylia is the abnormally small quantity of gastric contents found one hour after the test-breakfast. Biedert (“ Diatetik u. Kochbuch,” etc., 1895), who suffers from this affection himself, found that his stomach was very rapidly emptied, so that he had to draw the contents within forty-five minutes if he wished to obtain any at all. Julius Miller (/. c., “Archiv f. Verdauungskrankh.,” Bd. i,p. 233) found that strong solutions of sodium chlorid are very much diluted when they are brought into the human stomach. It is further known that strong solutions of common salt, when brought into the stomach, arrest HC 1 secretion. The tendency to dilute solutions that are put into the stomach is so persistent that it con- tinues even after the concentration of these solutions has inhibited the HC 1 secretion. Alcohol, various forms of sugar, dextrin, and peptone are absorbed, and a more or less active excretion of water goes on hand in hand and simultaneously with such absorption. In achylia gastrica, however, the stomach differs very much in this respect from the normal organ, since it has then lost its power of diluting the gastric contents. The fact that concentrated solutions of sodium chlorid inhibit the secretion of HC 1 has been made available in the treatment of hyperacidity. From this fact it is very probable that, in achylia, we are dealing not only with loss of the characteristic secretion, the gastric juice with its HC 1 and ferments, but also that there seems to be no secretion of any kind issuing from the mucosa. The diluting secretion of the stomach is, under normal conditions, not exclusively made up of the normal gastric juice, and we are here confronted with a physiological function of a very GASTRIC ATROPHY WITH ANEMIA. *53 complicated character, concerning which very little of a positive nature is known. There is a general consensus of opinion, which we can confirm, that in achylia there is an exceptionally great vulnerability of the mucosa. It is a frequent experience with achylic patients to find that particles of the mucosa showing slight hemorrhages are unintentionally scraped or torn off during the drawing of the test-meals. Lubarsch (/. c .), Einhorn (/. c.), Biedert (/. c .), Cohnheim (“ Archiv f. Verdauungskrankh.,” Bd. 1, p. 274), Jaworski (“ Munch, med. Wochenschr.,” 1887, Nr. 7 und 8), have observed this phenomenon, and the first-mentioned author asserts that the vulnerability of the mucosa in achylia is as great as in carcinoma. In achylia it is almost impossible to avoid the scraping off of portions of the superficial mucous membrane, no matter what shaped tube is used, and if it is desired to avoid scraping the mucosa at all, it is safer to use a tube which is entirely closed at its lower end and has but one velvet eye-opening at the side (Tiemann & Co., New York). Scraping off of minute particles is a harmless procedure, but the tearing of larger pieces by suction may be followed by extensive hemorrhages. Total loss of gastric secretion, even as a consequence of a fully developed atrophy of the mucosa (anadenia), can not cause anemia or cachexia per se. Those cases in which anemia has been observed in connection with achylia were most probably complicated by a mechanical insufficiency of the stomach, or by other diseases ; thus, in some cases, syphilis or tuberculosis, and extension of the atrophic process to the mucosa of the intestine, have complicated the gastric derangement. The credit of having first pointed out the association of gastric atrophy with anemia is usually attributed to S. Fenwick (lecture on “Atrophy of the Stomach,” “The Lancet,” July 7, 1877; also “ On Atrophy of the Stomach and Certain Nervous Affections of the Digestive Organs,” London, 1880, J. and A. Churchill). Both Einhorn (/. c., p. 321) and Martius (/. c., p. 16) assert that Fenwick’s report is the pioneer observation on this subject. As a matter of fact, it was our countryman, Austin Flint, who first called attention to the relation between anemia and atrophy of the gastric glands (Austin Flint, “ The American Medical Times,” 1 860). He expressed the opinion that some cases of profound anemia are dependent upon atrophy of the glands of the stomach. (The fur- ther contributions of Flint to this subject are to be found in the 56 854 ACHYLIA GASTRICA. “ New York Med. Jour.” for March, 1871, and in his “ Principles and Practice of Medicine,” p. 477, Philadelphia, 1881.) The pri- ority of Flint’s publications have been emphasized by Professor William H. Welch (“ A System of Medicine by American Authors,” vol. 11, p. 616 *). Although the anemia which supervenes in these cases of achylia can not be directly ascribed to the gastric atrophy, and too much importance was attributed by Flint and others to the state of the gastric mucosa, the reports of this author are, nevertheless, very valuable, because the secondary states, which we have men- tioned as really causing the anemia and cachexia, are most prob- ably brought about by, and owe their origin to, the primary degenerative changes in the gastric mucosa which Flint and Osier have described. In the first part of this work I have reported examinations of fragments of mucosa derived from twelve cases of anacidity or subacidity; of these, ten were cases of typical achylia gas- trica. In these twelve cases proliferation of glands, with marked round-cell infiltration, was found once. The fragment was appar- ently normal in two cases, but of the ten cases of typical achylia, granular gastritis and atrophy of the mucosa could be established in nine. In making the diagnosis of simple achylia gastrica we excluded all those cases of permanent loss of secretion evidently due to carcinoma or pronounced chronic atrophic gastritis. In fact, before making these detailed examinations, I supposed it was possible that this form of achylia existed simply as a neu- rosis, because all of the ten cases which we described occurred in neuropathic patients. I had also inclined to Einhorn’s view, that some forms of achylia might be of purely nervous origin. We have since then examined a number of new cases in addition to those reported, making in all fourteen. In none was the mucosa found perfectly normal. It seems improbable that a permanent * Since Flint’s publications, cases have been reported by Quincke, Brabazon, Noth- nagel, Rosenheim, and G. Meyer. The purely American contributions to this subject are very valuable. They have been made by Henry and Osier (“ Atrophy of the Stom- ach, with Clinical Features of Progressive Pernicious Anemia,” “ Amer. Jour. Med. Sciences,” April, 1887) ; F. P. Kinnicutt (“ Atrophy of the Gastric Tubules : Its Rela- tion to Pernicious Anemia,” “Amer. Jour. Med. Sciences,” vol. xciv, p. 419, 1887) ; Allen Jones (“Gastric Anacidity,” “New York Med. Jour.,” p. 573, May, 1893); D. D. Stewart (“ Amer. Jour. Med. Sciences,” Nov., 1895) ; Einhorn (“ Med. Record,” June 11, 1892) ; also in Boas’ “Archives of Digestive Diseases,” vol. 1, p. 158. ACHYLIA GASTRICA AS A CAUSE OF NEURASTHENIA. 855 cessation of a normal function could be caused by a neurasthenic condition. This explanation of achylia would be justifiable only in case we could demonstrate that in this affection the gastric mucosa was perfectly normal. To our knowledge, there is no case of well-authenticated achylia on record in which a cure or an improvement in the neurasthenia was reported to have cured or improved the secretory defect. There are, no doubt, highly nervous patients who secrete HC1 normally, but under the influence of the nervous excitement and apprehension coincident with the drawing of the test-meal, the gastric secretion is temporarily inhibited. I have seen three such cases in which I could not detect HC1 at six consecutive analyses, but a normal secretion was found in the vomited matter brought up by the patient at home. Later, the secretion was also found normal in the test-meals drawn at my office. The question has also suggested itself, whether achylia gastrica could not be the cause of the neurasthenia. Nor on this point are there any authen- ticated observations. Experience has taught, however, that neuras- thenic disturbances disappear in these cases with an improvement of the general condition, while the achylia continues, which would not be the case were the latter the cause of the neurasthenia. The loss of function in this disease is not a relative or transient one, but it is absolute and permanent. Biedert (/. c. f p. 173 ) gives it as his opinion that the persistent loss of HC1 and ferments gives the im- pression of a lasting defect, not of a variable increasing or decreas- ing inhibition. The absence of the gastric secretion is the same, whether the patients are very much run down and emaciated and subject to much suffering or whether they are in a state of good health. The supposition of Biedert that there may be a great many who possess this defect and are unaware of it, has been veri- fied by a number of observations among the students at my clinic. While studying the question whether the normal healthy stomach contained digestive juice in the fasting condition, we discovered an athletic, robust student who had no HC1 whatever in his stom- ach, whether fasting or after meals. The total acidity, taken after test-meals on six different occasions, varied between one and four; as these analyses were made shortly before the examinations for the degree of M.D., we did not inform the candidate of the physiological defect in his stomach, fearing that it might cause him some mental annoyance, and for all that we know he may still be unaware of his achylia and continue in vigorous health. 856 ACHYLIA GASTRICA. My results concerning the condition of the gastric mucous mem- brane are in accordance with those of Cohnheim (/. c.), Einhorn (“ N. Y. Med. Record,” June 27, 1896), Hayem (“ Allgem. Wiener med. Zeitung,” 1894, Nr. 2-17), and have recently been supported by Martius and Lubarsch (“ Achylia Gastrica,” pp. 1 12-170), and H. Strauss (“ Virchow’s Archiv,” Bd. cliv). The results of the very exact investigations of these last authors make it probable that a more or less pronounced granular gastritis exists in the majority of cases of achylia. The anatomical changes, however, are not, in all cases, suffi- ciently advanced to explain the permanent loss of function. There is no indication at present for determining whether glandular gastritis is the cause or result of achylia. It is self-evident that a weak gastric parenchyma should be less resistant to exterior detri- mental influences — such as bacterial invasion— than a robust gas- tric tissue. The secretion of HC 1 being the normal disinfectant, though not an absolute antiseptic, it largely protects the mucosa from infection. It is evident from what has been said in the etiology of the various diseases of the stomach that the organ is exposed to many external aggressions of a thermic, chemical, mechanical, and bac- terial nature, and it is a matter of astonishment what intense mal- treatment a healthy stomach will endure without reacting patho- logically. It is, therefore, conceivable that the anatomical loss of the glandular apparatus will render those individuals afflicted with primary simple achylia more susceptible to bacterial invasion. Most observers agree that the increased vulnerability of the mucosa goes hand in hand with the loss of secretion ; this lessens the power of resistance, and eventually induces a state of chronic granular gastritis, effected by causes which a healthy stomach would resist without any change. Symptoms. — The disturbances of function may long remain latent. Persons with achylia may for many years have no subjec- tive or objective disturbances of any kind ; but sooner or later dys- peptic complaints arise. The subjective sensations are not charac- teristic, but are essentially those of nervous dyspepsia, accompanied by eructation, fullness, and pressure after eating, gradually leading to attacks of severe gastralgia. The symptomatology, as based upon the complaints of the patient, is most accentuated in neuras- thenics. In persons with a perfectly sound nervous system achylia may exist, and the individual may be unaware of it ; this is proved SYMPTOMS OF ACHYLIA GASTRICA. 857 by the case of the medical student reported in the preceding. Oppler (“Deutsche med. Wochenschr.,” 1896, Nr. 32, S. 5 1 1 ) has reported a number of cases which make it probable that loss of gas- tric secretion predisposes to diarrhea and intestinal catarrhs, which are not benefited until the achylia is discovered, when rational treat- ment effects improvement. The personal description which Pro- fessor Biedert (/. c.) gives of his own case is a weighty argument pointing to the fact that achylic patients are very much predisposed to diarrhea. Among the achylic patients which I have studied (fourteen in all), I observed attacks of diarrhea in five. So far as I could determine, the colon and the duodenum were in normal con- dition. I also studied the state of the duodenum by my method of duodenal intubation, showing the pancreatic and hepatic secretions to be normal. This makes it probable that these diarrheas are pos- sibly not due to an extension of the anatomical changes in the stomach to the intestine, but to fermentative processes, developed in the absence of HC 1 secretion. These diarrheas confirm Bunge’s view that at least one effect of the HC 1 secretion is that of a par- tial antiseptic. Martius’ conclusions (/. c. } p. 101) are the following: Achylia gastrica is due to two conditions : (1) a primary secretory de- bility of the stomach, constituting simple achylia gastrica; (2) atrophy of the gastric mucosa (anadenia), which is secondary achylia gastrica. The primary achylia gastrica is either congenital or developed on the basis of a very early predisposition. It is associated with inherited debility of the nervous system, and pre- vails among so-called neuropathic patients. Primary secretory debility of the stomach is an individual peculiarity, which may remain latent for years, and without demon- strable detriment to the general organism. This is particularly the case when the motor function is well preserved, and the motor, secretory, and resorptive functions of the intestine continue normal. The mucosa, which is devoid of secretion, exhibits a diminished vital resistance to all external detrimental influences. This explains the fact that anatomical alterations of varying intensity are rarely absent in simple achylia gastrica. The structural changes bear no proportionate relation to the absolute gravity of the loss of function. It is, therefore, probable that there are forms of so-called atrophy of the gastric mucosa (the primary noncarcinomatous anadenia) 858 ACHYLIA GASTRICA. which develop preferably on the basis of this congenital secretory weakness of the stomach. Accordingly, there are gradual transitions, clinically and ana- tomically, from congenital simple achylia with but immaterial alterations of the mucosa, to achylia with chronic granular gas- tritis eventuating in complete atrophy of the secretory mucosa. The grave results for the total organism (progressive anemia, malnutrition, etc.) which have been ascribed to the latter type do not in reality develop until the mucous membrane of the intestine is extensively involved by the atrophy. Pathological Histology.— The investigations made by the authors quoted in the literature at the end of this chapter show in general a marked increase in the interstitial connective tissue. The surface epithelium contains many goblet cells. The vestibules to the glandular alveoli are very tortuous, and so dilated that they resemble minute cysts, filled with homogeneous, slightly granular masses, that stain with acid anilin. The epithelial cells lining the vestibules present marked variations in structure and staining qualities. Those most prominent are: (i) Ordinary, long, cylin- drical, epithelial cells. (2) Somewhat shorter, cylindrical cells with dark protoplasm and dark-staining nucleus, the upper end of which has disappeared. (3) Goblet cells. (4) Cells as in type 2, but with a very dark protoplasm (Stohr cells). (5) Cells with a marked fuchsinophilic granulation. In some vestibules only cells answer- ing to the description of type 2 are found, and in them an abund- ance of mitotic figures. In other vestibules we find goblet cells in addition to these. There are very few vestibules which contain normal surface epithelium. Among the other characteristics that were found in freshly hard- ened stomachs of achylic patients are : (1) Immigration and per- meation of leukocytes. (2) The occurrence of mitoses in the surface epithelium and in that lining the vestibular alveoli. The author’s cases were especially examined with regard to atypical or pathological mitoses, but the results were negative. (3) Occurrence of acidophilic leukocytes. (4) Frequency of goblet cells. (5) Occurrence of so-called Stohr’s and Nussbaum’s cells. (6) Occur- rence of hyaline spheres. Referring to No. 1 of the above observations, it should be stated that Sachs (“ Zur Kenntniss d. Magendriisen b. krankhaften Zustanden,” Breslau, 1886) has found an abundance of lymph-cells migrating through the surface epithelium and glandular substance. HISTOLOGICAL CHANGES IN ACHYLIA GASTRICA. The pyloric region seems to be more invaded than any other part of the stomach. Stintzing considers the immigration ofleukocytes in the normal stomach a very rare occurrence. Permeation of the gastric mucosa with leukocytes at the height of digestion is a normal occurrence, and has been frequently observed in animals. The difference in the achylic stomach, with regard to the permea- tion of leukocytes, is simply one of degree. Lubarsch found that the glandular lumina were actually packed full with acidophilic leukocytes; this property has not been found in the leukocytes of the normal stomach. It is probable that the invasion of the mucosa with acidophilic leukocytes to such a degree as Lubarsch describes is pathological. Concerning No. 2, the presence of mitoses in the epithelia of the normal stomach is denied by Sachs (/. c .) and Oppel (“ Lehrbuch der vergleich. mikroskop. Anatomie d. Wirbelthiere,” Bd. i : “ Magen”), and the occurrence of karyokinetic figures in the chief and border cells is extremely rare. For a closer study of the char- acter and significance of the mitotic processes I refer to my article (Hemmeter, “ Histological Studies Relating to the Early Diagno- sis of Cancer of the Stomach,” “ Phila. Med. Journ.,” Feb., 1900). The hyaline spheres which Lubarsch describes are composed of cell granules that have become confluent and enlarged, but are still contained within the body of the original cell. These hyaline spheres are considered pathognomonic for atrophic processes in the gastric mucosa. The histological changes found by various authors in achylia, and which we have been enabled to confirm in cases which we had opportunity to examine at autopsies shortly after death, in- dicate the proliferation of the interstitial connective tissue, the occurrence of acidophilic migrating cells; and, in addition, the disappearance of the specific glandular elements and cell prolifera- tion, emanating from the vestibules of the glands; also trans- formation of the gastric mucosa into intestinal mucosa. The pro- cess eventuates in complete atrophy of the mucosa. Einhorn has reported a case of achylia in which a bit of gastric mucosa was found in the wash-water, which under the microscope appeared normal. We obtained normal mucosa from two cases of achylia, when strips were cut from achylic stomachs running from the esophagus along the greater curvature to the duodenum ; on serial sections made at intervals of one inch apart, small areas of microscopically normal mucosa were found, particularly near 86o ACHYLIA GASTRICA. the cardia, while most other portions of the stomach showed distinct atrophic changes, with profuse immigration of leukocytes, and proliferation of the interstitial connective tissues. A small bit of mucosa accidentally found in the wash-water does not indicate the state of the entire stomach. When such normal fragments are found in achylia, it is still probable that other portions of the stomach may be diseased, and what may be a normal condition in a fragment from the fundus *or pyloric region, will be pathological for the intermediate zone (Martius and Lubarsch, /. c.; also Hem- meter, /. c .). We do not, therefore, consider the evidence satis- factory that achylia may exist with a perfectly normal gastric histology. In the great majority of cases of achylia, a progressive atrophic gastritis may be found to exist. There may be periods in the history of achylia when this condition exists without any apparent alteration in the gastric mucous membrane, and the fact that most patients do not consult the physician until the process has devel- oped to a very advanced state may explain the observation that the occurrence of achylia with perfectly normal stomachs is thus far supported by very few reliable microscopic examinations of gastric tissue fragments. All achylic patients give a history of years of gastric disturbances when they first present themselves for treat- ment, the anamnesis thus making it probable that the gastric changes must have progressed very far. In the case of the healthy medical student in whom we found achylia on six different exami- nations, we did not succeed in obtaining a piece of the gastric mucosa. In these cases frequent examinations for fragments of mucosa are necessary to decide the relation between the histological alteration and the clinical history. These examinations should be made at frequent and regular intervals, and in case of autopsies on achylic patients the stomach should be previously preserved by pouring in alcohol or Zenker’s fluid within a half hour after death, so as to prevent autodigestion. What relation exists between the atrophic process of the intestines and that of the stomach is un- known. It may be a direct continuation of the progressive gastri- tis, since it is very probable that the same detrimental agencies that cause the disease of the stomach give rise to the intestinal atrophy. One might assume also that excessive demands are made upon the digestive power of the intestines in the absence of the preparatory digestive function of the stomach. Again, it is probable that bacterial fermentations occur to a much greater degree when ETIOLOGY OF ACHYLIA GASTKICA. 86 1 the disinfecting power of the HC 1 is lost. In two autopsies on sub- jects who had shown the symptoms of achylia, the author observed that the coeliac axis, and all branches arising from it, were of un- usually small size. The gastric arteries were smaller than those of normal stomachs. The intestinal and mesenteric arteries were also smaller in diameter than normal. The dimensions of the hepatic and splenic arteries were smaller. The arteries of the heart, spleen, kidney, and liver appeared normal in size. On in- jecting the arteries of the stomach from the celiac axis, the diminu- tive caliber of the arteries was evident even without micrometric measurements. There was in this case no atrophic gastritis. Etiology. — Aside from the probability that achylia may be either congenital or developed upon a neuropathic basis, not much is known of the causation of the progressive atrophic gastritis. It has been supposed that bacterial infection is an etiological factor in bringing about this state of the mucosa. We may con- ceive the bacterial invasion to have occurred in a similar manner to that pictured under the head of ulcus carcinomatosum. In one of our drawings the presence of bacilli is represented beneath the floor of the ulcer, some of them located in the muscularis. (Plate VIII and Fig. 38, p. 532.) It is not known whether this bac- terial invasion is a cause or result of these processes. Syphilis and tuberculosis may be predisposing factors. Example of Clinical History. — Mr. L. W., thirty-two years old, reporter on a daily newspaper. Up to 1894 he was physically well and in good health, although he admits to have frequently abused his stomach by overeating and overdrinking. His mother is a highly neurasthenic woman, who imagines she is afflicted with all sorts of ailments; father, high-strung and arbitrary. His duties necessitate that he should be awake during the night and sleep during the day. As a consequence of this, he is compelled to take his meals at very irregular hours. He frequently does not obtain sufficient sleep, being awak- ened by noises in the street (trolley cars, etc.) and about the house in which he lives. He usually gets to bed about five o’clock in the morning, and, if his nerves are quiet, sleeps until eleven or twelve ; then, arising, he takes his break- fast. His main meal is taken between five and six o’clock in the afternoon. At seven o’clock he must report for duty as night clerk or reporter of the Asso- ciated Press. The work he has to perform is frequently of an exciting and enervating character. During the summer of 1894, while it was very hot, he had indulged in very cold beer during the night while following up some sporting occasion, and since then has suffered from dyspepsia, nausea, eructation, etc. Sometimes, after a meal, he will be attacked with palpitation of the heart and a feeling of giddiness, which has recently been associated with sensations of precordial fear. His appetite in the summer of 1895 was very poor ; the food 862 ACHYLIA GASTRICA. was described as weighing down his stomach like a lump of lead. Heart pal- pitation so strong that he can not sleep because of the noise his heart makes. In one month of the summer of 1895 he lost eleven pounds. Analysis of Test-meal . — The first test-meal had disappeared from the stomach entirely fifty-five minutes after it had been eaten. The second test- meal was drawn fifty minutes after it had been taken ; the amount was about three ounces, and it consisted of chewed particles of wheat bread entirely un- changed. Total acidity = 5 ; free HC 1 = negative ; combined HC 1 , negative ; lactic acid, trace ; propeptone and peptone, absent. On test by milk digestion, rennin and rennin-zymogen, absent ; pepsinogen, absent; very slight quantity of mucus ; very slight amount of filtrate gained by pressing the drawn ingesta through a sieve. Test of motor function, by the Hemmeter method, shows a rather increased peristalsis. Absorption (Penzoldt and Faber’s method) is abnormally delayed. Exam- ination of a fragment of mucosa shows irregular dilations of the peptic gland- ducts ; there is some increase of the interglandular connective tissue, which is infiltrated with tremendous numbers of leukocytes, which have also per- vaded the epithelial cells of the vestibules. Here and there the entire lumen of the gland-duct is packed full, and apparently pushed apart with an enormous invasion of lymphoid cells. The characteristic, spindle-shaped, connective- tissue cells are present, but unless carefully sought for, they escape detection, on account of a copious round-cell infiltration, and of the invasion of leuko- cytes, to which reference has been made. Many eosinophilic cells present. In the epithelia, cells with numerous chromosomes and others containing more than one nucleus. The nuclei in these cells are in various stages of indirect division, showing typical mitotic figures. Anatomical diagnosis, chronic granular gastritis. This patient improved very much after a vacation of six weeks in the summer, which brought him the necessary sleep at night and rest. Remedies to restore HC 1 secretion have been tried persistently for one year and six months without effect. He repeatedly suffered in the hot season of the year from attacks of diarrhea, which were easily controlled by administering HC 1 and subnitrate of bismuth, together with a proper diet. The patient has relapses whenever he indulges in over- work, with loss of sleep. Since 1895, twenty-three test-meal analyses have been made, not one showing a trace of HC 1 or ferments. Treatment. — At my clinic we are in the habit of prescribing dilute HCl for all these cases whenever the acid agrees well. As considerable HCl is needed to effect any appreciable digestive action and to exert a disinfecting influence, we give twenty drops of the official dilute HCl every half-hour after meals until sixty drops have been taken. The acid must be largely diluted and taken in a double gelatin (Aaron) capsule or through a glass tube. Our experience, which is based upon a large number of cases of this sort, has convinced us that the acid is not only well tolerated, but is almost indispensable to the patient. Although it may be argued that achylic patients sometimes get along without any DIET IN ACHYLIA GASTKICA. 863 treatment whatever, simply because they exhibit no symptoms, nevertheless when they do apply for treatment they generally present a complexity of symptoms, which are much benefited by carefully selected but nutritious diet, sometimes rest in bed, strych- nin, and HC 1 . When the appetite is absolutely lost, it may be restored by washing out the stomach with bitter tonics, such as gentian and quassia. In neurasthenic patients, strychnin sul- phate improves not only the local gastric symptoms, but also the symptoms of the general neurasthenia. A number of gastric patients of this kind refuse to eat, because they fear that distress will be caused by the food. In such cases it may become neces- sary to place the patient in a well-managed institution for the dietetic treatment of digestive diseases. They must gradually be convinced that food that is ingested with appetite can do no harm. When the motility is interfered with and symptoms of dilation are manifest, gastric lavage is indispensable. Concerning the use of pepsin and pancreatin see pages 344 and 345. Diet . — The achylic patient is an individual who has an internal infirmity, due either to a congenital defect, or to an acquired abnor- mality in the gastric structure. Whatever may be the condition and the cause, we are dealing with individuals who are essentially weak and debilitated. We have found it expedient not to be too exacting with diet orders. In fact, we make it a rule never to give a standing diet order to an achylic patient without carefully inquir- ing as to the food which he knows from experience agrees best with him. The stomach is a protective and selective organ, pre- paring the food for the intestines. By its selective property, when the motility is in a normal condition, it permits only the semisolid and liquid masses to pass first, while the more consistent masses are retained, to be further softened and disintegrated. We have shown, in the preceding pages, that the stomach of the achylic patient has lost the power to dilute its contents by a secretion from its walls. This is one of the main reasons why we permit the in- gestion of liquids during meals, and of largely diluted HC 1 after meals. For the same reason all foods should be well chewed, or preferably finely divided during the process of cooking, for the main object of all treatment must be to preserve the peristalsis , and to insure a healthy state of the mucosa. Therefore, the food should generally be taken in the form of gruels, pastes, or in any semisolid, easily swallowed state. The meat should be very soft, scraped, or run through the meat-grinder. Fish, sweetbread, 864 NERVOUS DYSPEPSIA. calf’s brain, and soft-boiled eggs are, as a rule, of such soft con- sistency that they need no further preparation. Our experience is that the more food is ingested and well tolerated, the better for the patient in these cases. We will give no outline here of detailed diet list, but refer the reader to the diet order for anacidity and Penzoldt graded diet order given in the chapter on Dietetics. In many cases physical and mental rest, hygienic surroundings, and a nourishing diet will be all that are needed for insuring comparative well-being of the patients. Where the motor power becomes de- fective, the treatment will be that outlined in the chapter on Motor Insufficiency. A remedy little known, but a very valuable adjuvant in treat- ment for lack of dietetic ferment, is the juice of fresh pineapple. This has decided proteolytic power, and, besides, is a pleasant, easily procured remedy. The ferment is only active in the fresh fruit, and is destroyed in the preserved pineapple. The name “ Bromelin ” has been given to the ferment by Chittenden (“ Journ. Physiol.,” xv, 1894). There is no treatment that is universally applicable to all cases of achylia. The ability of the practitioner in discerning the special indications for each individual case is put to the test severely in the therapeutic management of this disease. Sometimes the treat- ment will be that of chronic gastritis, sometimes that of nervous dyspepsia. Excessive strictness in dietetic regulation has, in the author’s opinion, occasionally developed gastric “ hypochondriacs.” It is more advisable to train up, or, as Broadbent says, “ level up,” the gastric digestion to a higher plane. We make it a rule to show these gastrophobic patients the contents of their stomach at a proper time after full meals, to convince them that they can digest thoroughly, for, as a rule, every vestige of food will have passed out of the organ within one and one-half hours. The literature on achylia gastrica will be found compiled in the article by Martius and Lubarsch, published by Franz Deuticke, Leipzig, 1897. DEFINITION OF NERVOUS DYSPEPSIA. 865 CHAPTER XIV. NERVOUS DYSPEPSIA (Leube).— NEURASTHENIA GASTRICA (Ewald). The original definition which Leube gave of this affection char- acterized it as a neurosis of sensibility, without any well-defined and constant objective disturbances of digestion, but exhibiting a large variety of subjective symptoms connected with the digestive act and occurring independently of any demonstrable changes in the stomach. In his first paper Leube (“ Ueber nervose Dyspepsie,” “ Deutsch. Arch. f. klin. Med.,” Bd. xxm, 1879) emphasized that the gastric digestion may be perfectly normal so far as the chemistry and motility are concerned, and that he has used the term “ dyspepsia,” or difficult digestion, because this act is accompanied by manifold complaints that are traceable to an abnormal excitability of the sensory gastric nerves. Since then Leube has expanded the con- ception of nervous dyspepsia to the effect that it includes anoma- lies of secretion and motility. R. Geigel and Abend (pupils of Leube) later on demonstrated that the secretion of HC 1 may be extremely variable in nervous dyspepsia, and that we may have a normal acidity, or euchlorhydria, subacidity, anacidity or achylia, or hyperacidity. Accordingly, the important symptoms of the trouble — viz., the annoying gastric dis- tress — can not be traced to fermentations of the gastric contents with sub- or inacidity, nor to the products of this decomposition, nor to irritation of the gastric nerves in superacidity. It is natural that the definitions and conceptions of various authors concerning a disease that is so vague and indefinite in its clinical history and pathology should differ greatly. Leube distinguishes more re- cently between two kinds of nervous dyspepsia : ( a ) Nervous dyspeptic symptoms in which the nervous channels are sympa- thetically involved by anatomical changes in the stomach, and altered chemistry of digestion caused by these changes. (/?) Ner- vous dyspepsia with an apparently normal anatomical state of the organ. Boas distinguishes a third form of nervous dyspepsia, which originates reflexly from other organs : for instance, the kid- neys, uterus, ovaries, male genito-urinary apparatus, and intestine. 866 NERVOUS DYSPEPSIA. Constitutional diseases, such as tuberculosis, syphilis, diabetes mellitus, anemia, uric acid diathesis, may form the basis of this complexity of symptoms. The disease may occur in an idiopathic form, independently of any demonstrable gastric changes, or in a secondary form consequent upon neurasthenia, hysteria, and the other pathological states referred to. Whatever the underlying basis or etiology of the disease, the ultimate symptoms can be as- scribed to a functional sensory neurosis and overexcitability of the gastric nerves, which may become so acute that they react in a pathological manner upon the influence of normal digestive stimu- lation. Pathology. — Jurgens has discovered total degeneration of the plexus of Meissner and Auerbach in forty-one cases of nervous dyspepsia. In one of the cases in which the sensory disturbances were predominant, and the intestinal functions involved also, this author found a distinct degeneration of the muscularis of the stomach and intestine. F urther exact pathological and histological investigation will very probably restrict the number of cases at present classed under nervous dyspepsia. The > conceptions of various authors concerning the nature of nervous dyspepsia vary considerably. Leube, as is well known, states that nervous dys- pepsia is of central origin, while Stiller applies the name to all digestive disturbances that are transmitted to the stomach through the central or the sympathetic nervous system. Stiller attributes greater importance than Leube to disturbances of the secretory function, which he could demonstrate in a majority of his cases. We interpret the disease as a mixed neurosis, in which the motor secretory and sensory nerve apparatus are affected contemporane- ously or alternately ; an anatomical substratum is present in one- half of the cases, but it is not of a constant type. Etiology. — Neurasthenia gastrica has been observed after intense emotional excitement, exhaustive mental work, alcoholic and sexual excesses, after abuse of tobacco, and associated with pul- monary phthisis, nephritis, and malaria. The sensibility of the normal gastric mucosa is very slight, and the digestive irritation causes no distinct sensation in the normal individual, but when a healthy person transgresses the customary amount of food, unpleas- ant sensations of pressure, distention, fullness, eructation, and nausea will ensue, indicating that the organ has been overloaded. These sensations cease when a part of the chyme has passed out into the intestine. SYMPTOMATOLOGY OF NEURASTHENIA GASTKICA. 867 Narcotic substances, such as very strong coffee, tea, or tobacco, may relieve or remove these symptoms, showing that they are of a purely nervous character. If the excitability of the sensory nerves is for any reason increased, then the normal digestive irrita- tion brings about such gastric difficulty. It is characteristic of nervous dyspepsia that gastric distress is perceived only after meals, and is absent when the stomach is empty. With an intensely excit- able nervous apparatus in the stomach, such symptoms as we have described may, in exceptional cases, come on even when the organ is empty. The nervous dyspepsia associated with malaria should induce the physician to examine the blood of the patient for the malarial parasite. The symptoms in these cases generally abate under the influence of quinin. As a secondary neurosis, neurasthenia gastrica is generally the result of general neurasthenia or hysteria. Grave anatomical alter- ations of the brain and spinal cord, which frequently bring on other gastric neuroses, are, so far as we know, not reported to have any causal relation to nervous dyspepsia. Reflexly, the disease may result from irritation arising from the genito-urinary organs in both sexes, from menstrual and puerperal disturbances. The dyspepsia during the puerperal period has been attributed to traction or compression of the sympathetic. In a portion of the cases it is impossible to attribute any cause. It is a disease which prevails among the male sex. Symptomatology. — The clinical picture of neurasthenia gas- trica is extremely variable. It is, therefore, impossible to give a well-defined, typical representation of the disease that can be applicable to the majority of the cases. We will, therefore, simply designate the most important and frequent symptoms. It is char- acteristic of nervous dyspepsia that the gastric distress is directly dependent upon the ingestion of food — that it occurs as a rule only after meals, and not on an empty stomach. Furthermore, it is characteristic that the quality and the quantity of the food and dietetic errors exert no influence upon dyspepsia. At times the most indigestible food causes no difficulty whatever, and at other times the most digestible food brings on distress. The sensations of the patient are very much under the influence of the emotional state. The dyspeptic symptoms are : Unpleasant sensations, pressure, fullness, distention of the stomach, occurring shortly after meals. After the patients have slept well, they are in a cheerful state of mind in the morning, but immediately after 868 NERVOUS DYSPEPSIA. breakfast they are tormented by manifold sensations in the stomach. The suffering is most severe when the neurasthenia gastrica is ac- companied by hyperacidity. In this case it increases during the second period of digestion, as the acidity becomes greater. Such types are relieved by the administration of alkalies, which, how- ever, are useless with achylia. The epigastric region is not very sensitive, nor are there any characteristic pain-points, so far as we could determine. Leven (“ Estomac et Carvau,” Paris, 1884) attributes great im- portance to the appearance of these so-called painful spots, which are supposed to be due to an irritation of the solar plexus. Burk- hart (“Pathol, der Neurasthenia Gastrica,” Bonn, 1882), Fleischer, Ewald, Bouveret, and Richter do not attribute much importance to this symptom. In some cases very peculiar sensations are de- scribed by these patients. Some have a crawling feeling in the stomach, as if some live animal were moving about in it. Some have a sensation of tickling, others describe it as a beating, burn- ing, or sticking sensation. A most unusual sensation is that de- scribed as a restless, wavy, or undulating motion. Persistent eructation is a very frequent and annoying symptom. The eruc- tations occur in an explosive manner, and without any regard for the surroundings. If there is hyperacidity, these eructations are accompanied by severe pyrosis. Emesis is rare, but when it does occur, the character and consistency of the vomit depend upon the composition of the gastric juice. With normal acidity or hyper- acidity it has a very sour taste and is void of proteid food when the acid is present in excess. With subacidity or inaeidity it con- tains much undigested meat and eggs and but little carbohydrate food. Although inacidity may be present, the gastric contents do not decompose, because there is no stagnation. The appetite is variable. There may be a normal appetite, bulimia, or anorexia. As a rule, thirst is increased. The behavior of the sensory gastric nerves is capricious. When the patient is in a cheerful, pleasant humor, or occupied with a congenial, interesting piece of work, he will digest articles of diet which will cause very great distress when he is emotionally depressed or otherwise indisposed. Exces- sive mental or bodily work, cares and worries concerning the vocation, disappointments in business enterprises, grief, etc., all cause a condition of excitability in which digestion is much impaired. Secretory Function . — In neurasthenia gastrica there may be a DIAGNOSIS OF NEURASTHENIA GASTKICA. 869 normal secretion, hyperacidity, or inacidity. When inacidity exists, the ferments can still be demonstrated in the gastric contents. This important fact will serve to distinguish this type of nervous dyspepsia from typical achylia gastrica. Motor Function . — The peristalsis of the stomach is in most cases undisturbed in neurasthenia gastrica, but there are cases in which temporary motor insufficiency occurs. Intestinal Disturbances . — The most constant symptom is obstinate constipation. Very frequently there are rumbling noises in the intestines and extensive flatulence. Nervous Symptoms . — These consist of pain and pressure in the head, giddiness, tinnitus aurium, flashes before the eyes, rapid pulse, exhaustion, cool extremities, attacks of fainting, palpitations of the heart, dyspnea. It is very probable that all these symptoms are connected with the deranged intestinal digestion, and that they are due to the absorption of toxic products formed during the putrefaction of food in the intestines. C. A. Herter and E. E. Smith (“ N. Y. Med. Jour./’ June 22 and 29, July 6, 13, and 20, 1895) have published clinical histories and detailed analyses show- ing the relations of psychical disturbances, melancholia, etc., to the toxicity of the urine. It is conceivable that the production of these symptoms, particularly frontal headache, beating in the head, congestions, pulsations of the large arteries, globus hystericus, mel- ancholia, and insomnia, is in some way related to excessive intes- tinal putrefaction. When the nervous dyspepsia is comparatively recent, the symptoms are limited to the gastro-intestinal tract, but when the disease is of long standing, the nervous symptoms may submerge the digestive, and it may be difficult to decide whether the latter or the former constitute the primary derangement. Diagnosis. — As a general rule, it will be found that the nervous dyspepsia is connected with some organic disease of one of the digestive organs. We refer to the various anomalies of position of the intra-abdominal organs that are described in the chapter on Gastroptosis and Enteroptosis. Frequently, dislocated kidneys, small tumors, herniae of the median linea alba, morbid changes in the male or female sexual organs, and organic diseases of the stomach and intestines, will be found to exist. There will be no connection between the quality and quantity of the food and the digestive difficulties, but sleep, emotional state, and psychical con- dition will be influential factors. The complaints of the patient are frequently described in exaggerated language. One of our patients, 57 870 NERVOUS DYSPEPSIA. who is the owner of a brickyard, describes his feelings as “ similar to the rolling of a ton of bricks in his belly” ; another compares his sensation to being “ stabbed with a red-hot knife ” ; still another describes her abdomen as being “ distended to bursting, like a bal- loon,” or, at other times, as feeling compressed as though it were in a vise. At other times these same patients, without recognizable reason, will make no complaints at all, will be very happy and cheer- ful, and digest well. These variations in the functional powers of digestion are very characteristic of nervous dyspepsia. Leube has called our attention to the emptiness of the stomach seven hours after a rather heavy test-meal. Prognosis. — Inasmuch as the course of the disease is a chronic one, it may, in severe cases, by continued and progressive loss of strength and emaciation, prove fatal. In those cases in which a cure has been effected relapses may occur, so that the prognosis should be guarded. Sometimes, when the fundamental disease is remediable, — for instance, in genito-urinary disturbances, malaria, etc., — or when the cause, such as sexual excesses, abuse of alcohol and tobacco, bodily and mental overexertion, can be removed, the resulting nervous dyspepsia may be permanently cured. Heterochylia (from erepos, meaning “ other ” or “ different,” and yuloq, meaning “juice ” or “ secretion ”). — This term is suggested by the author to denote a rapidly alternating state of secretion, occurring chiefly in nervous dyspepsia. In making a large num- ber of analyses in these cases, Dr. E. L. Whitney and the author have observed within one week that euchlorhydria, hyperchlor- hydria, and inacidity will be found after the same test-meals. In the discussion of a paper read before the American Medical Association, in Philadelphia, June 4, 1897, a colleague, Dr. E., of Brooklyn, stated that in his own case he had ;observed hyper- acidity and inacidity on the same day, after he had taken the identical meals and drawn a sample within one hour after they had been ingested. Dr. E., who is an able chemist, made quantitative analyses of his gastric juice on many occasions, and, so far as he can tell, these variations in the secretion are independent of his emotional state. In a number of the cases examined by Dr. Whitney and the author they found hyperacidity with rapid digestion of proteids, and defective carbohydrate diges- tion, with symptoms of pyrosis and eructation that were relieved by alkalies. Two days afterward the author examined the same cases, to find that two of them showed no reaction with Congo D I F FER ENT I A L D I A G NOS IS. 871 paper, no free nor combined HC 1 , and a pronounced HC 1 deficit. There was no pyrosis nor eructation, but the patients complained of a sense of fullness and weight in the stomach, together with anorexia, which symptoms were relieved by two doses of dilute HC 1 (thirty drops per dose). At the end of the same week we had occasion to examine the same cases again, and found the acidity normal. For want of a better expression we have designated these rapidly alter- nating states of secretion by the name heterochylia. When the acid is in excess, the proteids are absent from the test-meals, and rice and bread almost undigested. When the acid is absent, one may frequently find a defective proteid digestion but a rapid carbo- hydrate digestion. We have no explanations to offer for these cases beyond those which are purely hypothetical, but it is conceiv- able that a closer histological study of the finer ramifications of the gastric nerves, such as has been carried out with such admirable regard for detail by Henry J. Berkley in other organs of the body, may throw some light upon this puzzling phenomenon. For instance, we may sooner or later be instructed that the oxyntic or border cells receive a different nervous supply from the chief or central cells, or that both chief and border cells are supplied by nerves of widely differing character, one set exciting the function, the other inhibiting it, — i. e., anabolic and catabolic secretory fibers, — but all this is premature and problematic. Dr. Frank H. Murdoch, of Pittsburg, in a report to the American Gastro-entero- logical Association (Washington, May, 1898), gave a large number of analyses on cases of this type, showing a secretion varying from achylia to hyperacidity. Differential Diagnosis. — Nervous dyspepsia with inacidity may be confounded with chronic gastritis or carcinoma, and nervous dyspepsia with hyperacidity may be confounded with ulcer, while still other forms may bear a striking resemblance to atony or myasthenia. For the separation of chronic gastritis from nervous dyspepsia, the following facts are of importance : Chronic gastritis is accompanied more frequently by vomiting; the stomach con- tains large quantities of mucus and a few blood streaks; we may have also stagnation of the contents. The course of chronic gas- tritis is more uniform and typical, and the dyspeptic symptoms are directly influenced by the quality and quantity of the ingesta. In carcinoma the distress is present at all times, even on an empty stomach, vomiting is frequent, and the ferments are absent when the HCl secretion is lost. In nervous dyspepsia the ferments are Syz NERVOUS DYSPEPSIA. still present, though HCl may be absent. When symptoms of stenosis have occurred, there can be no difficulty about the diag- nosis. The differentiation of nervous dyspepsia from ulcer becomes difficult only in those cases in which there has been no hemat- emesis. The constant dependence of gastric pain upon the food, the sharply circumscribed pain-points in the epigastric region and in the back, are unmistakable criteria. We have spoken more fully of the differential diagnosis in the sections on the various gastric diseases with which nervous dyspepsia may be confounded. It must not be overlooked, however, that nervous dyspepsia may be associated with some form of organic gastric disease. Treatment. — The fundamental causes of disease should be hunted up, and, if possible, removed. The prospects of doing this are favorable if the cause can be found in the existence of intestinal parasites, floating kidney, malaria, and certain remediable diseases of the genito-urinary organs. In those forms of nervous dys- pepsia which depend upon an undue excitation of the nervous system, due to sexual excesses, abuse of alcohol and nicotin, or excessive mental and bodily exertion, improvement can not be hoped for unless these states are remedied. Patients must be impressed with the fact that drugs and other treatment will not improve them if they persist in their bad habits. Particularly American business men, who, with admirable energy, but with little regard for their own health, persist in executing work which is too severe for their mental and physical constitution, must be taught that the prime factor in successful treatment is rest ! This class of cases will, in the long run, prove to be very grate- ful patients if this truth is emphasized, and false expectations concerning the efficacy of drugs and washing out the stomach, etc., corrected at the beginning of the treatment. Better results can be obtained in all of these cases by a change of environment, with absolute psychical and physical quiet, removal from the cares and worries of business and household, than by the most detailed and complicated treatment. In connection with this we must emphasize the value of rational psychical treatment of nervous dyspepsia. The physician must, in a dignified manner, attempt to merit the absolute confidence of his patient. For this purpose we consider it important that he should show a warm, sincere interest in the suffering of his patients, even if, after a repeated and thorough examination, he should become convinced that the patient’s complaints are unreal and exaggerated. TREATMENT OF NEURASTHENIA GASTRICA. «73 It is a great comfort to these neurasthenics to listen patiently and sympathetically to their complaints, and not to ridicule or criticize them. The sufferings of the patient, psychically considered, are equally intense, whether they be real or imaginative. Gymnastics . — The author has frequently observed marked im- provement after a course of mild gymnastic training under an experienced training-master. The bicycle, moderately used, is a better means of promoting appetite and regular evacuations than drugs. In a similar way horseback riding, rowing, fencing, etc., are to be recommended. Climatic Treatment . — A sojourn in the mountains or at the sea- shore is a great help, inasmuch as it not only removes the patient from surroundings which maintain his disease, but at the same time insures rest, quiet, and, above all things, invigorating fresh air. In seeking a resort, fashionable places and those thronged with society should be avoided. The greater part of the day should be spent in the open air — if possible, in taking extensive walks. This will favor good sleep during the night. If there is persistent hyper- acidity with constipation, the patient will be benefited by a sojourn at Bedford Springs, Pa. Massage . — There is no doubt that massage improves the nutri- tion of the muscles and nerves, and favors a vigorous circulation, metabolism, and regular evacuation. Massage should not be per- mitted to be executed by the inexperienced. Nine-tenths of the persons claiming to be masseurs at the present time are charlatans. To be effective, the massage must be studied by the physician who has the case in hand, and though he may not execute it himself, he should, at least, supervise it. Hydrotherapy . — Cold sponge baths, taken in the morning imme- diately after arising, have a bracing effect. A good method is to wrap the entire body of the patient in a sheet dipped in cold water, and while the patient himself kneads and beats the parts of his body that are accessible to him in front, another person must per- form the massage of his back; after this the patient is thoroughly rubbed with a coarse Turkish towel. These cold rubs should not last longer than three minutes, after which the patient must dress and take a walk of about one mile. The favorable effects of hydrotherapeutic methods do not become manifest until they have been applied for two or three weeks. They are then followed by improvement in the appetite and sleep. When the insomnia is persistent, we are very fond of prescribing a warm salt bath, at the 874 NERVOUS DYSPEPSIA. temperature of the body, containing four per cent, of sodium chlorid and two per cent, of sodium carbonate. The patient is placed in this bath about half an hour before bedtime, and remains in it for about twenty minutes. In highly neuropathic patients the bath before bedtime has in my experience aggravated the insomnia — it should then be given about 4 p. m. Irrigations and Douches of the Gastric Mucosa . — These are used to reduce the hyperesthesia of the gastric nerves, and for this purpose carbonated waters are preferable to still waters. The gastric tube should be used which contains numerous small lateral openings instead of a few large terminal openings. If carbonated water can not be conveniently obtained, it can be prepared by adding citric acid or lemon juice to a one per cent, solution of sodium bi- carbonate. The amount poured into the stomach should not exceed twenty ounces at a time. Electricity . — Galvanization of the abdomen and the spinal region and general faradization are applicable in these cases. The faradic current should be applied to every muscle in the body, with large, broad, felt electrodes. A good method consists in placing the feet of the patient upon a large plate electrode (cathode), while the other pole is placed on the various muscle groups of the body. It is well to allow the large electrode to remain on the epigastric region for about five minutes, while the remaining one is passed up and down over the spinal column. The intensity of the current and the duration and localization of the treatment must be varied according to the individuality of the case. According to Erb, Beard, and Rockwell, this treatment improves the appetite and sleep, reduces the psychical irritability, and creates a more favor- able disposition to bodily exercise. Personally, we may, without defining the exact benefits derived from electric treatment, pro- nounce it to be an indispensable adjunct to the treatment of neuras- thenia gastrica. Perhaps it influences the nutrition of the nervous centers, or perhaps it is nothing but systematic massage. At all events, it effects an improvement in the sufferings of this class of patients. The Diet . — In this disease, more than in any other, the physician must see that the articles of food possess considerable variety and are well cooked and appetizing. The behavior of the digestive functions are so grotesque that it is impossible and useless to suggest stereotyped diet lists. Experience is the best guide, and the common phrase, “the proof of the pudding is the eating of MEDICINAL TREATMENT. 875 it,” is certainly applicable in these cases. It is very beneficial to the patient if he can take and well digest large quantities of milk; aside from its high nutritive value, milk acts upon the gastric mucosa like a soothing liquid ointment, and is a dietetic intestinal antiseptic. Sometimes when the patient is prejudiced against it, it is possible to mix it with the food surreptitiously, and our diet lists and “ dietetic kitchen ” give many formulas for this purpose. In the selection of the remaining foods, the taste, likes, and dislikes of the patient should be consulted so far as is consistent with rational dietetics. Articles of luxury, such as good fruit — grapes, pears, figs, dates, and, if anacidity exists, fresh pineapples — should not be forbidden. If constipation is obstinate, the diet should contain a large amount of these foods, and par- ticularly apples. Concerning the use of alcoholic beverages, no definite rule can be given. On the whole, we believe that wines and beer should be avoided, unless they are needed for stimulation and to improve the appetite. Large colon enemata with pure olive oil(300c.c. at a time) are sometimes curative in the nervous consti- pation, particularly the membranous colitis present in these patients. Perhaps the most effective treatment, on the whole, is that desig- nated as the Weir Mitchell rest-cure, a combination of hydrothera- peutic, electrical, and dietetic treatment, with gymnastics, rest, massage, and as much sleep as possible. When the state of the nutrition has been much reduced, the so-called “ Mastkur,” a sys- tem of fattening by highly nutritious diet and passive exercise, is, in our experience, very effective in bringing about a reduction of the symptoms and improvement in the digestive functions. This “ Mastkur” is not applicable to all classes of patients; those of an irritable and restless temperament and those who have organic gastric diseases are not improved by it. Drugs . — Those that have been employed in neurasthenia gastrica are the tonics, sedatives, and hypnotics. In anacidity the basic orexin, five grains three times a day, has been very much lauded by Penzoldt. The fluid extract of condurango, one teaspoonful three times a day, and the bitter tonics, calumbo, gentian, quassia, in doses of one dram three times a day, are sometimes of value, though personally we have seen no marked results follow their administration. The remedy we have most faith in is the sulphate of strychnin, of a grain three times a day continued for one month, at least. When malaria is associated with the nervous dyspepsia, quinin is the remedy “ par excellence.” Boas and 876 NERVOUS DYSPEPSIA. Einhorn speak very favorably of the use of bromids ; both of them employ mixtures of the ammonium and sodium bromids. While the remedies may have a temporary value and are indis- pensable for producing sleep and diminishing the excessive irri- tability of the nervous system, they must not be used continu- ously. We have assured ourselves, by quantitative analyses of the toxic products of the urine, similar to the studies of Herter and Smith (/. c.), that the toxicity of the urine is increased in nervous dyspepsia as soon as the total quantity of bromids admin- istered exceeds six grams in twenty-four hours. Maximowitsch recommends the following in neurasthenia gastrica existing on a basis of anemia : R . Ferri bromati, Chitlin bihydrobromic, aa 4.0 3 j. Ext. et pulv. rad. rhei, q. s. u. f. pil. No. CXX. M. SlG. — Two pills three times daily. The use of mineral spring waters is of doubtful efficacy. When an improvement is noticed at the mineral springs, it is probably due to the hygienic surroundings, the removal from care and worry and responsibility, and the discontinuance of the detrimen- tal habits encouraged at the home of the patient. For further con- sideration of the effect of mineral waters we refer to the chapter on this subject. If the insomnia is persistent, chloral may be unavoid- able. It should, in these cases, be given by rectal enema and not by the stomach. Fifteen grains in two ounces of starch water are usually sufficient to secure rest. An effective combination con- sists of five grains of chloral hydrate and eight grains of sulphonal. Opium and belladonna are best excluded from the treatment. Chloral even in very small doses (three grains at night) sometimes causes headache and lassitude the next day — it must then never be repeated. In uric acid diathesis and marked rheumatism the sali- cylate of soda (ten grains, t. i. d.) often produces not only relief of any existing pain, but even sleep. Sulphonal and trional are avail- able remedies for the insomnia, but, like the chloral, they have a deleterious influence upon the stomach, and should be preferably given per rectum. But the treatment producing the most lasting results is that which tones up and invigorates the neuromuscular apparatus and the nitrogen elimination and increases the will power. AUTHOR’S SYNOPSIS OF SCHEME FOR EXAMINING STOMACH PATIENTS AT THE UNIVERSITY OF MARYLAND 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 ? Intensely? 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? Diarrhea? Dysentery? Typhoid fever? Abdominal diseases? Menstrual irregularity? Pregnancies? PRESENT HISTORY.— Diseases of other organs? Pressure? Local and subjective com- plaints? Fullness? Pain? Distention? Restlessness? Sounds in the digestive tract? Bowel movements? Nausea? Eructation? Vomiting? Hematemesis? Appetite? Taste? Thirst ? LOCAL SUBJECTIVE SYMPTOMS. — Any difficulty or pain on deglutition? If so, its regu- larity? Intensity? Duration? Pain in stomach? Effect of food on pain? Does it 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? Deglutition sounds ? 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. — Occur on full or empty stomach ? Frequency? Taste of vomit? Appearance of matter ? Food particles? Proteids? Starches? Mucus? Bile? Pus? Blood? Food eaten several days before? Does emesis relieve symptoms? APPETITE AND THIRST. — Accustomed diet (let the patient state in detail what iseaten during the entire day)? Mode of life? Anorexia? Bulimia? Aversion to meat ? Thirst? BOWELS. — Constipation? Diarrhea? Undigested particles of food ? Mucus? Pus? Blood and source ? RESULTS OF BLOOD EXAMINATION. GENERAL NUTRITION. — Emaciation? Loss of weight in pounds? In what time? PHYSICAL EXAMINATION. Examination of Tongue, Teeth, and Mouth. INSPECTION. — Change of 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 ? Liver? Kidneys? PERCUSSION. — Limits of the stomach? DISTENTION WITH AIR OR GAS. — Limits of stomach? Results with intragastric bag? Does tumor move with distention? Made more or less distinct? ELECTRODIAPHANY. — Limits of stomach? Tumor? EXAMINATION OF TEST-MEALS. Double test-meal (see p. 121) — a full meal at say 9 a. m. Ewald test-meal at say 2 p. m. Contents drawn at say 3 P. M. Date, MACROSCOPICAL EXAMINATION.— (Quantity ? Color? Odor? Food particles ? Froth or gas? Pus? Mucus? Bile? Blood? Fragments of tissue ? MICROSCOPICAL EXAMINATION.— Bacteria ? Oppler-Boas bacilli ? Sarcinae? CHEMICAL EXAMINATION. — Reaction? Free acid? Free HC1 ? Lactic Acid? Amount freeHCl? Combined HC1? Amount acid salts and organic acids ? Total acidity ? Erythro- dextrin ? Biuret reaction ? Deficit of HC1 ? PEPSIN. Albumin digested in pure filtrate in. .. .minutes. Albumin digested in acidified filtrate in.... minutes. Albumin digested in HC1 and pepsin filtrate in minutes. RENNIN OR CHYMOSIN. Milk coagulated bj’ rennin in minutes. Milk coagulated by rennin-zymogen in minutes. Rennin-zymogen active in dilution 1. CONTENTS. — After meal previous evening at 8 p. M. CONTENTS. — After lavage previous evening at 8 p. m. TIME OF SALOL REACTION,. .. .minutes. TIME OF IODID OF POTASSIUM RESORPTION TEST,. .. .minutes. URINE.— Amount? Urea? Uric Acid? Reaction? Indican? Preformed sulphates ? Albumin? Tube-casts? Ethereal sulphates ? Ratio? Sugar? Specific gravity ? TREATMENT. Diet? Medicines? Electricity? Massage? Hydrotherapy? Lavage? Mineral spring water ? Gymnastics? Results? 877 LIST OF AUTHORS. Compiled by the author'' s pupils , Dr. Henry IV. Nolle and Air. Thomas II. Cannon. A. Abelous, bacteria in the stomach, 63 Adler, diseases of the heart and the stom- ach, 389 ; congenital atresia of the pylorus, 657 ; diet in hyperacidity, 829 Adler, Harry, carcinoma and Oppler-Boas bacillus, 564; gastroptosis, 730; hy- pertrophic stenosis, 614 Albu, autointoxication, 374, 798 ; coma carcinomatosum, 559 ; gastric tetany, 379 Alt, merycism, 769 Ames, phlegmonous gastritis, 434 Anderson, nutritive enemata, 206; absti- nence cure for ulcer, 514 Arnold, cancer, 565 Atkinson, digestibility of foods, 224 Atwater, dietaries, 24 ; effects of alcohol on metabolism, 289 B. Bachman, W. , amylaceous diet for hyper- acidity, 829 Bachmeier, floating kidney, 728 Baginsky, pepsin and trypsin interaction, 66 Bamberger, gastromalacia, 488 Bardenhauer, median hernia and gastral- gia, 800 Bardet, electric therapy, 303 Barie, asthma dyspepticum, 382 Bartels, gastric inflammatory atrophy, 450 Barthez, mtlaena neonatorum, 686 Baruch, Dr. Simon, natural mineral waters, comparative charts, 313 et seq. Basch, Seymour, gastralgia in tabic patients, 736 Bauer, rectal alimentation, 21 1 Beard, electric therapy, 302 Beaumont, peristalsis, 83, 84; stomach sur- gery, 348 Beck, cancer, 542 Bensley, histology and physiology of the gastric glands, 24 Bernabes, myoma, 609 Bernard, Claude, pancreatic juice, 55, 66 ; self-digestion of the stomach, 487 Bertlielot, steapsin, 57 Best, foreign bodies in the stomach, 61 1 Bettman, H. W. , malformation of the gas- tric cavity, 629, 643 Beynard, electric stimulation, 302 Biedert, HC1 therapy, 331 ; achylia, 852 Biernacki, kidney diseases and the stom- ach, 392 Bikfalvi, alcohol in digestion, 292 Billroth, surgery, 349, 350, 362 Bircher. Dr. Heinrich, gastrorrhaphy, 650 Blake, Dr. John D., gastralgia and adhe- sions, 658, 801 Blank, digestion of fats, 61 Boas, peptic gland cells, 23 ; ptyalin diges- tion, 45 ; duodenal chyme, 66 ; test- meal, 1 21 ; bile and duodenal secre- tion in stomach contents, 132; epithe- lial exfoliation, 137, 139; lactic acid test-meal, 161 ; analysis for HC1, method, 168; lactic acid estimation, 169 ; pepsin and pepsinogen tests, 174; rennin and rennin-zymogen esti- mation, 174; dietetics, 192,193,259; nutritive enemata, 205 ; diet lists, 232— 246; massage, 309; alkali therapy, 337, 340; gastric surgery and secre- tion, 358 ; asthma dyspepticum, 382 ; infectious gastritis, 438 ; gastritis acida, 458 ; ulcus carcinomatosum, 560 ; autointoxication in dilatation, 634 ; rumination with subacidity, 769 ; gastralgia, 799 ; gastric crises, 835 ; achylia gastrica, 854 Bocci, electricity, peristalsis and secretion, 302 Bollinger, glanders in the stomach, 590 ; foreign bodies, 612 Booker, W. D. , pathological gastric mucosa, 146 ; acute gastritis, 423 Borutteau, secretion and peristalsis, 90 Bottcher, infectious gastritis, 440 ; gastric ulcer, 490 Bouchard, gastric diseases and respiration, 376 Bouchert, papain, 346 Bouley, absorption, 91 Bouveret. artificial stomach distention, 99 ; gastric diseases and respiration, 376; 879 88o LIST OF AUTHORS. gastric secretion, 149 ; alcohol and tetany, 192 ; tetany and lavage, 299, 379 ; acute gastritis, 421 ; gastritis atrophicans, 460 ; nervous eructation, 755 ; bulimia, 810; gastric crises, 835 Brabazon, gastric inflammatory atrophy, 450 Brandi, gastric absorption, 93 Braun, organic acids, analysis, 1 70 Brenner, gastro-enterostomy, 350 Brigham, gastrectomy, 361 Brinton, gastric glands, 25, 26; peristalsis, 8 5 Broadbent, Sir Wm. H., anorexia, 191 ; motor insufficiency, 842 Brock, galvanism and gastric neuroses, 306 Brooks, valvulse conniventes, 33 Brown-Sequard, the stomach in nervous diseases, 385 ; gastromalacia, 489 Briicke, pepsin determination, 174 Brunner, peristalsis testing, 71 Bryant, Joseph D., cancer statistics, 545 Bunge, HC 1 an antiseptic, 63 Burkhardt, dietetics, 207, 208, 249 ; neur- asthenia gastrica, 868 Burton, pancreatic juice, 56 Bush, digestion in the absence of the usual ferments, 215 C. Cabot, Richard C. , examination of gastric contents for blood, 135 Cahn, predigested food, 209 Cannon, peristalsis, 85, 87 Canstatt, electric therapy, 303 Capelle, foreign bodies in the stomach, 612 Captain, gastric bacteria, 63 Cartellieri, eructation, 754 Charcot, gastric crises, 735 ; anorexia, . 8l 5 Chiary, hour-glass stomach, 645 Chittenden, Prof. R. H., saliva, 1 7 1 ; composition of beef products, 199 ; alcohol in digestion, 290 Chomel, diet in dilation, 202 Chomele, dilation. 637 Christomanos, antiperistalsis, 213 Church, food energy, 227 Chvostek, purulent gastritis, 437 Cohnheim, Paul, mucosa fragments, 82 ; • achylia gastrica, 853 Cohnheim, ulcer, 489, 490 ; cancer, 541 Colin, absorption, 91 Connor, Dr , gastric surgery, 348 Contejean, peristalsis and secretion, 90 Cornil, diagnosis of cancer, 563 ; lymph- adenoma, 590; polypi, 607 Courvoisier, gastro-enterostomy, 349 Cruveilhier, polypi, 608 Cseri, massage, 309 Czerny, resection, 349 ; pyloroplasty and resection, 364 D. Daettwyler, gastric ulcer, 491 Dauber, antiperistalsis, 213 Davis, gastropexy, 365, 730 Debove, secretion of the stomach, 149 Decker, gastromalacia, 489 Deininger, gastric abscess, 437 Deiters, predigested foods, 209 Delafield, acute gastritis, 423 Devic* gastric fermentation and tetany, 192 ; tetany from lavage, 299, 379 Dobson, Nelson C. , ulcer, 515 Dock, George, cancer, 562 Donders, dietetics, 185 Donkins, H. B., nutritive enemata, 206; abstinence cure for ulcer, 514 Dreger, George R. , electrical stimulation, 82 Dubey, hypertrophic sclerosis, 445 Duchenne, electrotherapy, 303 Dujardin-Beaumetz, carbohydrates in hy- peracidity, 196; dietaries, 221 Duret, gastropexy, 365, 730 E. Earl, Dr. Samuel F., tuberculous rectal fistula, 389 Eberth, carcinoma, 563 Ebstein, nervous diseases and the stomach, 385 ; gastromalacia, 489 ; polypi, 608 Edinger, L. , acute gastritis, 422 Edkins, acid and formation of pepsin, 27 ; absorptions, 91 Edsall, D. L., gastrosuccorrhea, 845 Eichhorn, subcutaneous feeding, 219 Eichhorst, peristalsis testing, 71 ; spectro- scopic examination for blood, 135 ; rectal alimentation, 2 II ; dietetics, 238 ; acute gastritis, .428 Einhorn, Dr. Max, gastric motor function, 71 ; gastrograph, 74; mucosa exfolia- tions, 82; gastrodiaphany, 104; stom- ach bucket, 120 ; erosions of the stom- ach, 137, 140; their pathological sig- nificance, 141 ; gastric secretion in the fasting state, 149, 150; intragas- tric spray, 300 ; electrical stimulation, 302, 304, 305 ; intragastric electrode, 3°3 > gastritis, 415 ; electricity in chronic gastritis, 472 ; trauma and ulcer, 491 ; hypertrophic pyloric ste- nosis, 614; frequency of dislocated kidney, 721 ; gastrosuccorrhea, 843 ; achylia gastrica, 850, 854, 856 Eiselberg, von, pylorectomy, 360; phyto- bezoar, 613 Elsasser, gastromalacia, 488 Emmerich, bile action, 60 Engel-Reimers, cysts, 610 Escherich, bacteria in digestion, 62, 69 LIST OF AUTHORS. 88 I Ewald, capacity of the stomach, 1 8 ; fer- ment action, 46, 66; peristalsis, 71; test-meal, 121, 122 ; mucosa exfolia- tions, 135, 140; secretions from the fasting stomach, 149, 150; nutritive enemata, 211 ; diet list, 231, 238; massage, 309 ; formula for anorexia, 341 ; tetany, 380; nervous diseases and the stomach, 385; abscess, 437; gastromalacia, 489 ; syphilitic ulcer, 601 ; foreign bodies in stomach, 61 1 ; fatal gastric hemorrhage, 688 ; bu- limia, 807 F. Faber, absorption, 92 Faust, action of pepsin on proteids, 176 Fenwick, Samuel, insufficiency of secre- tion, 330 ; gastric inflammatory atro- phy and anemia, 853 Fenwick, W. Soltau, poisoning by lavage, 299 ; pulmonary diseases and the stomach, 387 ; melsena neonatorum, 685 Fermaud, gastritis parasitaria, 440 Finlder, papain, 346 Finney, J. M. F., exploratory laparotomy, 694 Fischer, melsena neonatorum, 686 Fitz, R. H., phantom tumor and dilation of the colon, 725 Fleiner, electrodiaphany, 106; test-meals, 1 21, 122; alcohol and tetany, 192; carbohydrates in hyperacidity, 196 ; gastritis, 41 5; sarcomata, 547 Fleischer, gastric motor function, 71 ; per- istalsis, 72 ; gastrodiaphany, 104 ; diet-list, 246 ; HC1 combining power of foods, 247; gastritis, 415; men- struation and gastric disturbances, 736 Flexner, Dr. S., tubercular ulcer, 591 Fliess, gastric neuroses, 207 Flint, Austin, HC1 as a medicinal agent, 33° 5 gastric inflammatory atrophy, 449 ; anemia and atrophy, 853 Foote, El M., ulcer, 515 Foster, gastromalacia, 488 Fowler, intravascular feeding, 218 P'ox, Wilson, ulcer cure, 512; hyperacid- ity and peptic ulcer, 501 Frankel, A., asthma dyspepticum, 383 ; fatal gastric hemorrhage, 688 Frankel, C., acute gastritis, 427 Frerichs, gastric glands, 26 Friedenwald, Dr. Julius, acidities after test meals, 122 ; toxic products in gastric diseases, 374, 634 Fubini, electricity, peristalsis, 302 G. Gafifky, infectious gastritis, 458 Galeotti, diagnosis of cancer, 563 Gftrtner, bacillus of melena, 686 Gerhardt, C., eroded mucosa, 136; ulcer, 287 ; gastritis parasitaria, 440 Gersung, dietetics in stenosis, 204 Gessner, bacteria as ferments, 61 Gillespie, interaction among bacteria, 63 ; gastric motor function, 71 ; gastric douche, 728 ; absorption from the stomach, 747 Glaevecke, absorption of iron, 816 Glax, purulent gastritis, 434 Gluczinski, test-meal, 121 Gmelin, tryptophan, 57 ; bile test, 132 Goldschmidt, electricity, peristalsis, and se- cretion, 307 Golgi, mucosa histology, 24 Gombauldt, hypertrophic sclerosis, 444 Graaf, Regnier de, intestinal contents, 52 Gros, Dr. A. P. , rest of the digestive or- gans, 285 Grutzner, digestive action of the succus entericus, 68 ; rectal alimentation, 21 1, 212 Grynfelti, melaena neonatorum, 686 Gull, anorexia, 815 Gussenbauer, gastric surgery, 348 H. Haberkant, Dr., gastric surgery, 348; statistics on surgical operations, 354, 37 °> 373 Habershon, statistics on gastric ulcer, 494 Hacker, von, gastro-enterostomy, 350, 352, 359, 3^3 > gastro-anastomosis, 365 ; surgery for ulcer, 515 ; NaCl infusion for gastric hemorrhage, 516; hour- glass stomach, 645 Haeberlin, cancer statistics, 545 Hahn, gastrolysis, 351 ; surgical treatment, 359 > 363 Haig, Alexander, rest of the stomach, 286 ; gout of the intestines, 391 Halliburton, W. G. , pancreatic juice, 56 Halliday, Andrew, merycism, 768 Hamilton, Dr. Alice, tuberculous ulcers, 593 Hammarsten, rennin-zymogen test, 51 ; composition of bile, 59 ; bile action, 65 Hammersclilag, test for peptonizing power of gastric juice, 173 Hanot, hypertrophic sclerosis, 444 Hanseman, mitosis in diagnosis of cancer, 563 ; tumors, 613 Hartung, mucosa fragments, 136 Hauser, cancer, 541 ; ulcus carcinomato- sum, 560 Hayem, mucosa pathology, 140 ; anemia, chlorosis, and gastric diseases, 386; “ gastrite hyperpeptique,” 844; achylia gastrica, 856 882 LIST OF AUTHORS. Hehner-Seeman, organic acid estimation, . ! 7 ° . Heidenhain, peptic gland-cells and their secretions, 22, 23, 24, 48; function of bile, 60 Heinecke, von, pyloroplasty, 363 ; puru- lent gastritis, 437 Heinsheimer, metabolism in gastro-enter- ostomy, 369 Hemmeter, Dr. John C., duodenal intuba- tion, 52; intestinal putrefaction, 64; gastric motor function, 71 ; peristalsis, 74, 87, 90 ; gastrograph, intragastric stomach-shaped rubber bag, 76, 79, 82, 89; test for absorption, 94-97 ; entero- and gastro-diaphany, 105, 108, 1 12; double-current stomach- tube, 1 16 et seq.; acidity after test- meals, 124; significance of mucosa exfoliations, 141-145 ; digestibility of foods, 187 ; digestion of enemata, 213; dietaries, 232, 236; alcohol and gastric motility, 293 ; electric stimula- tion, 304 ; formula for anorexia, 340 ; gastrectomy, 361 ; gastric tetany, 381 ; kidney disease and the stomach, 392 ; phlegmonous gastritis, 434; chronic hypertrophic gastritis, 443 ; electricity and chronic gastritis, 472 ; gastro- malacia, 487 ; gastric ulcer treatment, 512 ; cancer statistics, 546 ; ulcus car- cinomatosum, 560 ; carcinoma, early diagnosis, 566 ; duodenal intubation, 622-642, 670; Rontgen-ray photog- raphy of the stomach, 641 ; deter- mination of length of the esophagus, 655 ; pathogenesis of enteroptosis, 706 ; histology of stomach-glands in hyperacidity, 734 ; absorption of iron, 815 ; proliferation of glandular ele- ments in hyperacidity, 817 ; hyper- acidity, 822 ; achylia gastrica ; 859 ; merycism, 769 ; pyloric sounding, 773 ; schema for examination of stomach patients, 877 Hemmeter, Mrs. J. C., dietetics, 281 Henne, HC 1 therapy, 33 1 Henoch, asthma dyspepticum, 381 ; the tongue in chronic gastritis, 455 Henry, red corpuscles in carcinoma, 404 ; gastric atrophy and anemia, 854 Hensen, Hans, bacterial invasion of the digestive tract, 64 Herschel, absorption, 93 Herter, nervous dyspepsia, 869 Heryng, transillumination, 105, 106 Herz, malaria and gastric hemorrhage, 685 Hildebrandt, gastritis parasitaria, 440 Hippocrates, dietetics, 185 Hirschler, carbohydrates and putrefaction, 68 H odder, intravascular feeding, 218 Hodge, C. F. , effect of electricity on nerve elements, 301 Hoffmann, secretion in the jejune stomach, 148, 150 ; electricity and secretion, 302 ; gastritis, 447 Hofmeister, peristalsis, 83 Honigman, dietetics, 194; HC 1 therapy, 330 Hoppe-Seyler, gases in the stomach, 405; effect of exanthematous diseases on the gastric mucosa, 415 Horner, gastralgia and lipoma, 800 Howell, W. H., amylolysis, 46 ; peris- talsis, 83 Huber, peristalsis test, 72 ; gastric secre- tion, 149, 150; rectal alimentation, 21 1 ; dietetics, 238 Hiif ler, gastrodiaphany, 104 Hunter, autodigestion of the stomach, 487 Huseman, infectious gastritis, 438 Hutchinson, pulmonary diseases and the stomach, 388 J- Jacobson, diaphany 106, 107 108 Jaksch, von, rectal contents, 68 ; detection of blood, 135 ; carbohydrates and hyperacidity, 196; on the diazo re- action, 428 ; coma carcinomatosum, 559 Jaworski, rennin test, 51 ; colon contents, 67; test-meal, 121 ; secretion stimu- lation, 150; secretion and peristalsis after gastric operations, 358 ; catarrhus acida, 844 ; achylia gastrica, 853 Johnson, Dr. R. W., gastric surgery, 842 Johnson, Wyatt, acute gastritis, 427 Jones, Allen A., gastric secretion, 150; electrotherapy, 306 ; renal diseases and the stomach, 393 ; anacidity, 854 ; gastralgia, 597 Jones, Bence, urinary changes in stomach- diseases, 407 Jurgens, nervous dyspepsia, 866 Jiirgensen, Chr., amylaceous diet in hyper- acidity, 829 Justesen, J., amylaceous diet in hyper- acidity, [829 K. Kaiser, surgery, 348, 568 Kansche, surgical treatment, secretion, and peristalsis, 358 Karst, subcutaneous feeding, 219 Kaufman, Oppler-Boas bacillus, 1 30 Kazzander, valvulae conniventes, 33 Keen, Prof. W. W., gastric surgery, 350, 675 ; ulcer statistics, 518 ; gastropexy, 730 Kelly, Dr. H. A., gastric surgery, 761 LIST OF AUTHORS. 883 Key, Axel, ulcer, 490 Kinnicutt, F. P. , gastric atrophy and anemia, 330, 854 Klebs, ulcer, 489; cancer, 542 ; infectious granulomata, 593 Kleinwachter, acute gastritis, 429 Klemperer, peristalsis, 71, 72; test-meal, 121 ; acute gastritis, 422 Klikowicz, alcohol in digestion, 292 Knapp, uterine displacements as a cause of nephroptosis, 714; frequency of dislocated kidney, 721 Koch, nervous diseases affecting the stomach, 385 ; gastromalacia, 489 Kolliker, gastric glands, 25 Kooyker, foreign bodies in the stomach, 612 ICorcynski, catarrhus acida, 844 Kramer, stomach operations, 358 Kraus, the mouth in gastritis, 456 Kretschy, menstruation and gastric dis- turbances, 736 Krompecher, cancer-diagnosis, 563 Krueg, subcutaneous feeding, 219 Kuhn, F., absorption, 94; HC1 action on yeast, 15 1; predigested foods, 209; gases in the stomach, 405 ; pyloric sounding, 642 Ktihne, trypsin and pepsin interaction, 66 Kundrat, infectious gastritis, 439 ; sarco- mata, 547 et seq. Kupffer, border cells in fundus, 23 Kussmaul, alcohol and tetany, 192 ; diet in dilation, 202; gastric douche, 299; electric therapy, 303 ; gastric tetany, 379 ; stenosis of the duodenum, 660 Kuttner, diaphany, 106, 107, 108 ; gastric surgery, 350 L. Lambl, polypi, 608 Lancaster, fatal gastric hemorrhage, 683 Landau, splanchnoptosis, 717 ; mekena neonatorum, 685 ; etiology of floating kidney, 696 ; intestinal stenosis, 719 Landenberger, hypodermic feeding, 219 Landois, dietetics, 220 Langerhans, recognition of gastroptosis, 104 ; etiology of enteroptosis, 702 Langermann, HC1 therapy, 331 Langley, ferment and acid cells, 27 ; pepsin and trypsin interaction, 66 Larrey, stomach surgery, 348 Lauenstein, gastro-enterostomy, 349 ; gas- trolysis, 351 Lauterbach, asthma dyspepticum, 382 Lebert, infectious gastritis, 438 Legroux, transfusion for hemorrhage in ulcer, 516 Lemoine, alkali therapeutics, 334 Leo, secretions in the fasting stomach, 149 ; estimation of IIC1, 167; estimation of fatty acids, 1 70; bulimia, 807 Leonard, diagnosis of renal calculus, 804 I .eroy, transfusion in hemorrhagic ulcer, 516 Lctulle, ulcer, 490 Leube, peristalsis, 71 ; test- meal, 121 ; gastric secretion test, 150; nutritive enema, 21 1 ; subcutaneous feeding, 219; dietaries, 241; alkali therapy, 334 > gastric and intestinal vertigo, 378 ; acute gastritis, 428 ; gastric ab- scess, 4}7 ; gastromalacia, 488 ; ulcer cure, 512 ; nervous dyspepsia, 865 Leven, nervous dyspepsia, 868 Levertin, absorption, 96 Lewin, bacterial invasion of the walls of the digestive tract, 64 Leyden, dietetics, 194, 204; alcohol and metabolism, 289 ; juvenile vomiting, 760 Leydig, gastric glands, 25 Lindner, gastric surgery, 350 Linossier, therapeutics of alkalies, 234 Litten, chronic gastritis, 460; dislocation of the kidneys, 710 Littmann, papain, 346 Lobker, pyloroplasty and pylorectomy, 363 London, ulcer, 489 Loreta, digital divulsion of pylorus, 364 Loye, electrical stimulation, 302 Lubarsch, O. , insufficiency of gastric se- cretion, 329 ; achylia gastrica, 850 Luclcsdorf, bacteria of mouth and intestine, 63 Ludwig, electricity and 1 the motor func- tion, 302; mineral springs, 313 et seq. Liittke, HC1 determination, 166 M. MacDonald, gastrectomy, 361 Macfayden, bacteria in economy of diges- tion, 62; ileum contents, 67 Macleod, abscess, 436 Magendie, vomiting, 756 Maisoneuve, surgery, 349 Malbranc, gastric douche, 299 Mall, F. , anatomy of the stomach, 17; peptic gland cells and their secre- tion, 23, 25, 27, 90; antiperistalsis, 216 Maly, HC1 formation, 48 ; bile and putre- faction, 60 Mannaberg, sustenance of colon bacteria, 70 Marfan, stomach in pulmonary diseases, 387 Martin, interaction of secretions, 66 ; gastric absorption, 93 ; detection of sarcinse, 129 ; gastritis, 415 ; anthrax gastritis, 439 ; ulcerations, 491 884 LIST OF AUTHORS. Martius, secretions in the fasting stomach, 148, 149; HC1 determination, 166; insufficiency of secretion, 329, 330, 850 Mathieu, total quantity of gastric contents, 150; gastritis, 415 ; acidity of the urine and gastric contents, 820 Mayer, gastric vertigo, 378 ; autodigestion, 488 McCall, treatment of ulcer by nutritive enemata, 206 Meckel, J. E., vertical position of stomach, 697 Mehring, von, starch digestion, 46 ; gas- tric absorption, 65, 91, 93, 95, 191 ; analysis for fatty acids, 172 Meinert, acute gastritis, 429 Meisenbach, foreign bodies in stomach, 613 Meltzer, S. J., electrical stimulation, 79, 305, 364; absorption, 91 ; electricity in chronic gastritis, 472 ; subphrenic abscess, 5 11 ; congenital pyloric ste- nosis, 657, 660 Meltzing, gastrodiaphany, 107, 108 Mendel, alcohol and digestion, 290 Mensche, bitter tonic treatment, 340 Menzel, hypodermic feeding, 219 Merrem, stomach surgery, 348 Meschede, gastritis parasitaria, 440 Mesnil, du, alkali therapy, 334 Metschnikoff, interaction among bacteria, 62 Meyer, G , HC1 in gastric therapy, 330 Michaelis, gastric hemorrhage, 516 Michel, gastric hemorrhage, 5 15 Mikulicz, gastroscopy, 178; statistics in gastrectomy and gastrotomy, 353 ; pyloroplasty, 363 Miller, mouth microbes, 63 ; absorption, 95 Milliot, transillumination, 104 Minassian, H. A., merycism, 768 Minkowski, bacteria in the stomach, 130 dietetics, 202 Mintz, HC1 as a remedial agent, 331 ; pylorectomy, 359 Mitchell, Weir, fattening rest cure, 207 Miura, alcohol as a food, 288, 289 Morau, HC1 in gastric antisepsis, 63 Moritz, stomach support, 19 ; intragastric apparatus, 76, 82 ; circulation of gas- tric ingesta, 89 ; dietetics, 194 Morris, Henry, gastrotomy, 352 Moss, analysis of a man, 220 ; percentage nutrition of foods, 224 Muller, peptone test, 177 ; intestinal auto- intoxication, 375 Munk, J., bile and absorption, 60 ; prepar- ation of food, 193 Murphy, surgery, 368 Murray, lipoma, 608 N. Naunyn, abnormal retention of ingesta, 201 Nencki, bile, agency of, in pancreatic diges- tion, 60; fat decomposition, 61 ; bac- teria in digestion, 62 ; ileum contents, 67 Neubauer, absorption, 97 Neumeister, schemata of digestion : amylol- ytic, 46 ; proteolytic, 49, 58 ; biliary diastatic ferment, 59 Noorden, von, deficiency of gastric juice and health, 329 ; HC1 therapy, 330 ; malnutrition, 374 ; gastric crises, 757, 835 Nothnagel, antiperistalsis, 212, 213; in- sufficient secretion, 330 ; gastric in- flammatory atrophy, 450 Novarro, gastro-enterostomy, 367 Nuttal, bacteria, not essential to digestion, 62 O. Obalinski, secretory and motor functions as affected by surgical operations, 358 Ogata, albumin as food, 209 Oppel, anatomy of the stomach, 17; gas- tric glands, 25 ; achylia gastrica, 859 Oppler, gastrodiaphany, 109 ; sarcinae, 129 ; asthma dyspepticum, 382 ; achy- lia gastrica, 857 Oppolzer, gastromalacia, 487 Orth, acute gastritis, 422; infectious gas- tritis, 439 ; gastritis polyposa, 445 ; carcinoma, 527 et seq. ; infectious granulomata, 590 Oser, infectious gastritis, 438 ; faradic cur- rent in gastralgia, 805 Osier, gastric atrophy and pernicious anemia, 330, 854; carcinoma, 368; acute gastritis, 416, 428 ; chronic gas- tritis, 450; abdominal tumors, 554, 555 > 558 ; tubercular ulcer, 592 ; dila- tion, 637; splanchnoptosis, 720 Ott, infusion treatment for ulcer, 516 t P. Pancanowski, location of the stomach, 779 Panecki, gastralgia and the uterus, 800 Panum, gastromalacia, 489 Park, Roswell, cancer, 543 Pasteur, bacteria in digestion, 6 1 Pavy, self-digestion, 488 Pawlow, innervation of gastric glands, 48 ; 738 ; secretory nerve of pancreas, 48 ; gastric secretion, 197 Pean, resection, 349 Pedioux, cutaneous diseases and the stom- ach, 396 Penzoldt, absorption, 92 ; stomach- tube, 1 17; dietetics, 194, 203; dietaries, 228-231, 235, 241 ; bitter tonics, 339 ; LIST OF AUTHORS. 885 gastritis, 415 ; dilation, 631 ; hunger, 814 Pepper, effect of electricity on peristalsis, 302 ; dilation, 637 Perco, hypodermic feeding, 219 Perry, E. C\, intestinal stenosis, 719 Petruscky, tuberculous ulcer, 515, 594 Pettenkofer, bile-acid demonstration, 133 Peyer, bulimia, 809 ; gastralgia and genito- urinary diseases, 800 Pliaff, bile, 59 Pick, secretion in the empty stomach, 148; gastritis, 416 ; autointoxication in di- lation, 634 Pitt, lymphadenoma, 609 Playfair, fattening rest cure, 207 Podwyssozki, pepsin production, 27 Posner, bacterial invasion of bowel wall, 64 Potain, asthma dyspepticum, 383 Preuschen, von, melaena neonatorum, 686 Pribam, gastric vertigo, 378 Prudden, acute gastritis, 423 Q. Quincke, insufficient secretion, 330 ; chronic gastritis, 450 ; ulcer, 491 R. Rachford, digestion in the duodenum, 330 Ranke, bile, 59 Ranvier, lymphadenoma, 590 Rauber, villi, 34 Reaumur, stomach contents, 52 Reiche, hour-glass stomach and ulcer, 510 Reichert, alcohol as a food. 288 Reichmann, transillumination, 106; gastric secretion, 149 ; HC 1 as a medicinal agent, 331 ; alkali therapy, 336 ; bitter tonics, 339 ; gastrosuccorrhea, 334, 836, 858 Remond, stomach secretion, 149, 150 ; hour-glass stomach, 643 Remsen, Ira, mineral spring water, 470 Richards, Mrs. E. H., rations, 225 Richardson, gastrectomy, 361 Richet, acid and pepsin, 28 Rieder, cancer, 562 Riegel, peristalsis test, 71 ; determination of location, Size, and capacity of the stomach, methods, 9, 102, 106; test-meal, 121 ; sarcinse, 1 29 ; Oppler- Boas bacillus, 130; secretion in the ■ fasting stomach, 149 ; nutritive ene- mata, 206, 212; predigested foods, 209 ; gastric douche, 3C0 ; massage, 309 ; hyperacidity and ulcer, 501 ; HC1 in therapeutics, 330; bitter tonics, 340 ; asthma dyspepticum, 381 ; hypersecretion, 832, 840 58 Rillet, melama neonatorum, 685 Rindfleisch, ulcer, 490 Ritter, gastromalacia, 489 Roberts, Sir William, effects of cooking on food, 250; “indications of the palate,” 251 ; alcohol in digestion, 292, 296, 297 ; hyperacidity, 818 Rockwell, electrotherapy, 302 Rohmann, bile and intestinal peristalsis, 60 Rokitansky, gastromalacia, 488 Rollet, gastric gland cells, 22, 26 Romeyn, alcohol and metabolism, 289 Rondeau, myoma, 609 Roseman, alcohol and metabolism, 289 Rosenbach, asthma dyspepticum, 381 Rosengarth, Jos., pathogenesis of entero- ptosis, 702 Rosenheim, gastric cells, 22 ; stomach- tube, 1 1 7 ; gastroscopy, 178, 181, 184; pancreatic ferment, 215 ; gastric douche, 299; massage, 309; secre- tion and the motor function following surgical operations, 358 ; gastritis, 4 1 5 ; chronic gastritis, 450 ; carcinomatous ulcer, 510, 560 ; carcinoma diet, 575 ; gastralgia and median hernia, 800 Rosenstein, stomach in diabetes mellitus, 391 Rosenthal, hydrotherapy, 308; anorexia, 815 ; gastroxynsis, 834 Rosin, secretion in the jejune stomach, 148 Rossbach, gastroxynsis, 834 Rossi, electric stimulation to secretion, 302 Rotch, acute gastritis, 421 Roth, gastralgia and median hernia, 801 Roux, W., proteids and carbohydrates in hyperchlorhydria, 196 Rummo, carbohydrates vs. proteids in the treatment of hyperacidity, 196 Runeberg, artificial stomach distention, 99 Rupp, resection, 361 Ruysch, cysts, 610 Rydygier, resection, 349 S. Sachs, achylia gastrica, 858 Salkowsky, absorption test, 97 Salzer, Henry, test-meal, 121, 124 Scammell, relative value of foods, 223 Schafer, absorption of fats, 56 Schech, the mouth in gastritis, 456 Scheperlen, chronic gastritis, 450 Schetty, acute gastritis, 422 Schiff, pepsin and acid, 27 ; gastric ulcer, 488 ; stomach in nervous diseases, 385 Schillbach, electricity and peristalsis, 302 Schlatter, gastrectomy, 361 Schlesinger, Oppler-Boas bacillus, 130; sarcoma, 546 886 LIST OF AUTHORS. Schmidt, Adolph, digestibility of mucus, 1 31 ; mucosa in gastric diseases, 146 ; alcohol and metabolism, 289 Schmidt, F., gastric fever, 427 Schmidt, H., nephroptosis, 714 Schmidt, John, frequency of dislocated kidney, 721 Schonborn, foreign bodies in the stomach, 611 Schreiber, secretions in the fasting stom- ach, 148, 149, 836, 840; dilation, 457 5 gastrosuccorrhea, 838 Schreiner, Dr. E. R., diet-list, 192 Schuchardt, pylorectomy, 360 Schiitz, peristalsis, 83 Schwartz, infusion of salt solution in hem- orrhage from ulcer, 516 See, Germain, test-meal, 121 ; alkali treat- ment, 338 Sehrwald, physiology of cells, 23 Seifert, the mouth in gastritis, 456 Senator, asthma dyspepticum, 384 ; gas- tritis parasitaria, 440 Senn, N., gastric distention with hydro- gen, 367 ; bone plates, 368 Shaw, L. E., intestinal stenosis, 719 Sieber, bacteria in the digestive economy, 62, 69 ; contents of ileum, 67 Sievers, gastric motor function, 71 Silbermann, asthma dyspepticum, 381 ; ulcer, 489 ; melsena neonatorum, 686 Simon, Chas. E., indican in gastric dis- eases, 197 ; HC 1 therapy, 332 ; urine in stomach-diseases, 410 Smith, E. E., neurasthenia gastrica, 869 Sohlern, von, carbohydrates vs. proteids in hyperacidity, 196 Sohnan, gastric functions affected by surgi- cal operations, 358 Spalteholz, gastric anatomy, 17 Stammreich, alcohol and metabolism, 289 Stansfield, gastro-enterostomy, 368 Stein, absorption from the stomach, 747 Stern, stomach in heart-disease, 389 Stewart, D. D., neuroses, effect of elec- tricity on, 306 ; ulcus carcinomatosum, 560; relation of anemia to gastric atrophy, 854 Stiller, enteroptosis, 702 ; pylorospasm, 746; nervous vomiting, 759 ; hunger, 806 ; nervous dyspepsia, 866 Stintzing, dietetics, 203 Stockton, Chas. G. , neuroses — electricity, 3 ° 3 > 3°6 Stokes, chronic hypertrophic gastritis, 445 Strauss, Herman, lavage, 120 ; total acid- ity, 123; gastric secretion, 150; lac- tic acid test, 168; diet in hyperacid- ity, 829 ; achylia gastrica, 850 Streit, gastric operations, 358 Strieker, ulcer, 487 Strobe, mitoses in gastric carcinoma, 563 Strumpell, asthma dyspepticum, 381 Swieten, von, dilation, 202 Swiezicki, von, cell physiology, 23 Swiezynski, antiperistalsis, 213 T. Talma, hyperesthesia toward HC 1 , 333 ; gastric ulcer, 489 Tanchon, cancer statistics, 544 Tappeiner, gastric absorption, 91, 93 Thierfelder, bacterial relation to digestion, 62 Thomas, T. G., intravascular feeding, 218 Thompson, Gilman, food classes, 43 ; die- tetics, 193 ; intravascular feeding, 281; dietetics of alcohol, 288; min- eral springs, 313 et seq. Tinker, ulcer statistics, 515 Topfer, free H Cl estimation, 163 Treheux, acidity of the urine and gastric contents, 820 Trousseau, gastric vertigo, 377 Turck, F. B., bacteria, 128; pyloric intu- bation, 642 U. Uffelmann, lactic acid test, 161 j; dietetics, 193 V. Velden, von der, secretion, gastric, in neo- plasms, 550 Virchow, erosions of mucosa, 136; ulcer, 488, 489 ; splanchnoptosis, 707 ; en- teroptosis, 708 Vogel, absorption test, 97 Voit, bile, 59, 60 ; rectal alimentation, 3 11 Vulpius, gastralgia and median hernia, 800 W. Waldeyer, cancer, 540 Wassmann, gastric glands, 25 Weber, guaiacum test, 134 ; electricity as a stimulus to peristalsis, 302 Wegele, dietetics, 194 et seq.; electric therapy, 303 Weir, Robert F. , ulcer, 515 Welch, William H., chronic gastritis, 450 ; ulcer, 494, 495 ; carcinoma, 537 > vicarious hemorrhage from stomach, 683 ; nephritis and fatal gastric hem- orrhage, 685 ; idiopathic gastric hem- orrhage, 687 ; achylia gastrica, 854 Welti, ulcer, 489 Westphalen, gastro-enterostomy, 479 Whitney, Edward L. , gastric absorption, LIST OF AUTHORS. 887 97 ; chemistry of gastric digestion, 148 et see].; the blood and urine in stomach-diseases, 400-413; gases of the stomach, 404 ; heterochylia, 870 Whittaker, subcutaneous feeding, 219 Widal, acute gastritis, 427 Wiel, dietetics, 193 Williams, pancreatic juice, 66 Winniwarter, von, surgical treatment, 348 Winslow, Professor Randolph, gastroplica- tion, 365 Wisting, von, bile function, 60 Wittich, bile, 59 Witzel, gastrotomy, 352 Wolf, L., bitter tonics and secretion, 339 Wolfler, surgery, 349, 362, 365 Woltering, dietetics, 194 Woodruff, C. E., food rations, 227 Wurtz, papain, 346 Y. Yeo, dietetics, 194 ; food energy, 226 Yeo, Burney, gout and dyspepsia, 391 Z. Zabludowsky, massage, 309, 3 1 1 Zawadski, secretion and peristalsis in sur- gery, 358 Zawardsky, pancreatic secretion, 56 Zesas, gastrostomy, 353, 368 Ziegler, acute gastritis, 423, 434 Ziemssen, von, gastric secretion, 180 ; elec- tricity and secretion, 302 ; hydro- therapy, 308 ; massage, 309 ; gas- tritis, 472 ; ulcer, 512 Zweifel, pancreas diastase, 56 ; gastric absorption, 93, 94 LIST OF SUBJECTS. Compiled by Dr. Henry IV. Nolle and Mr. Thomas II. Cannon . A. Abdominal regulatory center, 378 Abscess, gastric (see Gastritis, Phleg- monous) ; subphrenic, 510 Absorption : of various substances, 65 ^de- pendence on the motor func- tion, 70, 90; variations in, 90 ; testing methods, 92 ; a conditioning factor in diet, 189, 191 ; influence of alcohol, 2 94 Acetic acid : intestinal fermentation, 61 ; analysis, 163 Acetone, 412 Achlorhydria, 850 Achroodextrin, 45, 46 Achylia gastrica : nature and concept, 850 ; symptoms, 856; patho- logical histology, 858 ; etiology, 861 ; treatment, 862 Acidity: as affected by test-meals, and climatic, barometric, and geo- graphic factors, 122, 123, 124; of the urine and gastric contents, 820 Acids: acetic, 61, 163; action of succus entericus, 61 ; amido-, 42, 61 ; asparaginic, 57 ; aspartic, 58; bile, 65 (detection in stomach contents), 132 ; butyric, 57, 61, 162 ; caproic, 61 ; carbonic, 61 ; diacetic, 412; fatty, 57, 61, 170; fatty, quantita- tive estimation of, 170; free (tests), 156 ; hydrochloric (see Hydro- chloric Acid) ; lactic, 61, 130, 160, 168, 169, 564, 565 ; nitrogen-free vegetable, 42 ; organic free, 48 ; organic total (estimation), 170; oxyacids, 6 1 ; phenylacetic, 61 ; phenyl propionic, 61 ; skatol car- bonic, 61 ; stomach acids (analysis), 163 ; valerianic, 61 Acoria, 81 1 Adenocarcinoma, 527 Adenoma, pedunculated, 610 Albumin, acid (see Syntonin) Albuminoid decomposition, 67 Albuminous substances (see Proteids and Albumins) Albumins: digestion — peptic, 48, 49 ; tryp- tic, 57, 58 influence on biliary secretion, 59; bile action on, 60 ; re- lation to succus entericus, 60 ; in treatment of hyperse- cretion and hyperacidity, 194- 198, 246, 247, 248; in urine the result of gastric disorders, 412 Albumoses, 62 Alcohol : in food substances, 42 ; an intes- tinal fermentation product, 6 1 ; gastric absorbability of, 65 ; diet- etics, 287 ; effects of, on meta- bolism, 289 ; action of, on peptic digestion, 290 ; action of, on pan- creatic digestion, 292; action of, on salivary digestion and on the motility, 293 ; absorption affected, 294 ; summary of action, 294, 295 ; in certain pathological states, 295 ; Sir Win. Roberts’ theory in respect to alcoholic re- tardation of digestion, 296 Alimentation, rectal (see Enemata, Nutri- tive) Alkalies, medicinal agents, 334 Alkalinity of the blood, 403 Alkaloids, 42 Alveoli, 21 Amidulin, 45, 46 Ammonia, 61 Amphopeptone, 49, 58 Amylaceous foods in hyperacidity, 194- 198, 248, 828; in hy- persecretion, 248, 828 Amylodextrin, 45, 46 Amyloid degeneration of the stomach, 464 Amylolysis : bile in, 66 ; hyperchylia, its influence on, 718 ; pancreatic, 56 ; ptyalic, 44-47, 60 Amylopsin, 56, 66 Anacidity : dietetics, 198 ; indol formation and putrefaction, 332 890 LIST OF SUBJECTS. Anadenia ventriculi, 850 Analysis : stomach contents, technic, 114, 1 16; methods, 127; quantitative chemical, 15 1 ; of gastric juice, 156; of stomach acids, 163, 17 1 Anemia and gastric affections, 386, 512, 853 . Anorexia, nervous: dietetics, 190; the clinic of, 814 Antipeptone, 58 Antiperistalsis, 211-213 Antisepsis of the digestive tract, 47, 64, 249 Antizymotics (see agents under Anti- sepsis) Antrum pylori, 18, 83 Appetite, anomalies of the sensation of, 806 Asthma dyspepticum, 381 Atony : gastric, myasthenic : terminology, etiology, etc., 624, 625, 629 ; differential diagnosis, 639 ; prog- nosis, 642 ; treatment, dietetic, 201, 207, 235 ? . 237, 645-652; medicinal, etc., 645- 6 47 gastric, neurotic : definition and etiology, 774-776; symptomatology, 776— 781 ; prognosis and diagnosis, 781 ; treat- ment, 781-786 (see Dietetic under Myas- thenic Type) Atresia, 643 Atrophy of the stomach, 850 Auerbach, plexus of, 38 Autochthonous vegetation, 63 Autodigestion, gastric, 487 Autointoxication, intestinal, 65 B. Bacteria : fermentation and putrefaction, 56,61,66, 68, 130; economic and pathogenic significance, 62, 64, 128-130; species, 61, 62- 69, 120, 439 ; source of food for the colon flora, 69 ; analysis of stomach contents for, 128, 129 ; in the walls of the stomach, 128 ; HC 1 and peristalsis as re- lated to propagation of, 128; products giving rise to patholog- ical conditions, 130 Bag, intragastric, stomach-shaped, of Hem- meter, 76, 79-82, 89 Basement membrane, 34, 35 Bile : composition, 59 ; uses and functions, 59, 60, 65, 66; detection, 132 Blood: supply to the stomach, 28-31; supply to the intestines, 32, 34, 37 ; in stomach contents, tests for, 1 33, 134; in gastric diseases, 400- 404 Boas’ method, analysis of stomach acids, 168 Braun’s method, 1 70 Bulb for aspirating test-meals, 117 Bulimia : dietetics, 189 ; nature, 806 ; causation, 808 ; symptomatol- ogy, 809 ; diagnosis, 810 ; treat- ment, 813 Butyric acid : steapsin digestion, 57 ; in putrefaction^ 61 ; analysis, 162 C. Calcium, 42 Cancer (see Carcinoma) Carbohydrates : economic function, 42 ; effect on bile efflux, 59 ; absorption of, in presence of bile, 60; fermentation, 61, 62, 67 ; action of the succus entericus, 69 ; in hyperacidity and hyper- secretion, 194-198, 247, 248, 829 Carbolic acid, 61 Carbon, 41 Carcinoma : germ growth in walls of stom- ach in, 128; blood changes, 404; pathology, 527; eti- ology, 540 ; symptomatology, 547-561 ; diagnosis, 561-575 ; treatment, 203, 240, 568, 570, 572, 576; indications for operation, 356 ; prognosis, 577 ; differential diagnosis (see Table), 587 ; adeno-, 527 ; col- loid, 535; duodenal, 558; medullary, 530; pancreas, 557 ; scirrhous, 533, 534 Cardia : anatomy of the, 18 ; carcinoma of the, 566; obstruction of, 652 ; ob- struction of, forms of, 653 ; symp- tomatology, 654; diagnosis, 654; prognosis, 655; treatment, 655; cramp of the, 739 ; incontinence of the, 764 Cardiospasm, 739 Caroid, 346 Casein, 51, 57 ; peptones, 57 Catarrh, gastric, 234, 235, 443 Cecum, 40 Celiac axis, 28 ; plexus, 38 Cells : acid, 24 ; adelomorphous, 22 ; anilin-staining, 24 ; border, 22, 23, 24, 27, 28 ; central, 22-24, 2 7> 2 $ ; LIST OF SUBJECTS. 89I chief, 22-24, 25, 26; columnar epithelial, 21, 32, 35 ; cuboidal epithelial, 21 ; cylindrical epi- thelial, 22; delomorphous, 23; eosinophilic, 35 ; epithelial of villi, 35,61; ferment, 24; goblet, 36; mucous or mucin, 21, 22, 26; neoplasm, 562 ; Nussbaum’s, 23 ; oxyntic, 22, 23; parietal, 22, 23; pyloric gland, 25 Cerebral vomiting, 756 Chlorids: in gastric HC1 production, 49 ; in urinary changes, 408 Chlorin, 42 Chlorosis and gastric diseases, 386 Cholelithiasis, 509 Chyme, 55, 59, 65, 66 Chymosin (see Rennin) Cirrhosis: gastric, 614; ventriculi, 445, 553 Clinic, the gastric, 414 Clysters (see Enemata) Colon, 40; diaphany, 105; observations on dislocation of, 698 Coloptosis, 724 Coma carcinomatosum, 559 Constipation, chronic, dietetics in, 245 Convulsions of the pylorus, 746 ; of the stomach, 748 Cooking, dietetical, 253 Coprostasis, 709 Coronaria ventriculi artery, 30 Cramp of the cardia, 739 ; of the pylorus, 746 Creatin, 42 Crises, gastric, 757 Cysts, gastric, 610 D. Deutero-albumoses, 58 Deuteroproteoses, 49 Dextrin : digestion product, ptyalic, 45, 46, 47 ; amylolytic, 56 ; absorption of, 65 Dextrose, 45-47 Diabetes mellitus and state of the stomach, 39 1 Diagnosis, differential, of cancer, ulcer, gastralgia, hyperchlorhydria, and gas- tritis (see Table), 587 Diaphany of stomach, 104; colon, 105; duodenum, 105 ; ileum, 106 Diarrhea, chronic, diet, 243-245 Diastase : of saliva, 44, 45 ; in bile, 59 ; of pancreas, 56, 66 ; as a medic- inal agent, 343 Diazo reaction, Ehrlich’s, 413 Dietetic exercise, 283 Dietetics : historical retrospect, 185 ; diges- tibility, 186; gastric functions conditioning diet, sensation, 189 ; absorption, 19 1 ; secre- tion, 194; motility, 201 ; hyper- secretion and hyperacidity, 194- 198 ; anacidity or subacidity, 198; ulcer, 195,205; gastritis acida, 195 ; ulcus carcinomato- sum, 195, 203; atony and dila- tion, 201 ; carcinoma, 203 ; neuroses, 207 ; fattening cures, 207; predigested foods, 208; rectal alimentation, 210 ; intra- vascular and hypodermic feed- ing, 218; tables of dietaries, 220; diet lists, 228; cooking of food and the palate, 250-254 ; rectal enemata, varieties of, 280 ; alcohol and alcoholic bev- erages, 287 ; drinks and liquid foods, 254 Diet lists : Penzoldt’s, for the gradual training of the digestive ca- pacity, 228 ; Ewald’s and Boas’, 231 ; Hemmeter’s, chronic gastritis, etc., 232 ; Wegele’s, chronic catarrh, 234 ; Wegele’s gastric atony, 235, 237 ; Hemmeter’s, for anacid dilation, 236 ; carci- noma, 240 ; ulcer, 241 ; chronic diarrhea, 243 ; hyper- acidity, 246 ; hypersecretion, 247 ; intestinal antisepsis, neu- rasthenia, and neuroses, 249 ; and dyspepsia on hysterical basis, 249 Digestion : alcohol retardation of, theory of Sir William Roberts, 296 ; amylolytic, 44, 47, 56, 59, 66 ; fat, 57> 59 5 intestinal, 52, 70, 826; pancreatic, 55, 58, 292; peptic, 47-52, 290, 295, 296 ; proteolytic, 47-52, 58 ; pty- alin, 44, 45, 60, 171, 293 ; ren- nin, 51, 174, 175 ; salivary, 44, 45, 171, 293; starch, 45, 46, 47, 56, 60; steapsin, 57; tryptic, 57, 58 Digestive disturbances in connection with renal diseases, 394 Dilation, gastric : classification and nomen- clature, 624; obstructed form, 625 ; differential diagnosis, 639 ; progno- sis, 642; treatment, 201, 235-238, 647, 652; atonic form, 629 ; differ- ential diagnosis, 640; treatment, 201, 236, 237, 645, 652 ; diagnosis by gastrodiaphany, 106-108 Dilator pylori, 20 Dimethyl-amido-azo-benzol test, 157 Disinfection of digestive tract, 47, 64, 249 Divulsion, digital, of the pylorus, 364 Douche, the gastric, 299 892 LIST OF SUBJECTS. Drinks and liquid foods, 254 Duodenal intubation, 52-55 ; secretion, interaction, 65, 66 ; secretion, detection, 133 Duodenodiaphany, 106 Duodenum, 31, 32, 38 Dyspepsia, nervous : nature and concept, 865 ; pathology and etiology, 866 : symp- tomatology, 867; prognosis, 870 ; diag- nosis, 869 ; hetero- chylia, 870 ; differ- ential diagnosis, 871 ; treatment, 249, 872 E. Elastin, 47, 57 ; peptones, 47, 57 Elastoses, 57 Electric stimulation of peristalsis, 79-82 Electricity in gastric therapy, 301 et seq. Electrodiaphane, 105 Electrodiaphany, 104-112; criticism and limitations of the method, 108-1 1 1 Electrode, intragastric, Einhorn’s, 303 Enemata : dilation, 202 ; evolution of, 210; ulcer, 205 ; antiperistalsis, 2 1 2, 21 3 ; digestion of, 214 ; prepara- tion and administration, 216, 217; indications for nutritive kind, 217; kinds of nutritive, 280 Enterodiaphany, 105 Enteroptosis : etiology and symptomat- ology, 695-7 1 1 ; historical view of, 700 : treatment, 726 Enzymes (see Ferments) Epileptiform convulsions, 379 Erosions, gastric, dietetic treatment, 205 Eructation, nervous, 754 Erythrodextrin, 45, 46 Esophageal applicator, 183 ; forceps, 183 ; tubal probe, 1 21 Esophagoscope, 183 Ethereal oils, 42 Ewald tube, 124 Examination of stomach patients, schema, 877 F. Faradization, 304, 306 Fasciae teniae, 40 Fats : economic import, 43 ; in pancreatic digestion, 57; effect on flow of bile, 59; bile action, 60 ; action on suc- cus entericus, 60 ; bacterial action, 61 Fatty acids: pancreatic digestion, 57; bacterial product, 61 ; analysis, 1 70 Feeding, rectal (see Enemata, Nutritive) Fermentation : relation to the economy, 62; products, 61, 67; in- hibiting agents, 128; in gastrectasia, 15 1 Ferments: amylolytic, 44, 45, 56, 60, 66, 17 1, 342; amylopsin, 56, 66; artificial, 342 ; bacteria (see Bacteria); diastatic, 44, 45, 56, 59, 66, 343; inverting (of succus entericus), 60 ; milk- precipitating (pancreatic), 56; pancreatic diastase, 56 ; pan- creatin (medicinal agent), 344 ; pepsin (see Pepsin) ; pepsin- ogen (see Proenzymes) ; pine- apple, 347 ; proteolytic, 49, 57, 213; prozymogen, 25, 26; ptyalin, 44, 45, 60, 171, 342; rennin (see Rennin) ; rennin- zymogen (see Proenzymes) ; steapsin, 57, 60 ; trypsin, 58, 66, 67, 68, 69, 70; interaction, 65, 70; tests, 171 ; in urine, 413 Fibromata, 606 Food substance : constituents, and their relation to the economy, 41, 42; food groups of Gilman Thompson, 43 ; kinds of food values, 43 ; combining power with HC 1 , 248; drinks and liquid foods, 254 Foreign bodies in the stomach, 610 Fundus of stomach, 18 Fungi (see Bacteria) G. Galvanization, 306 Gases: acetylene, 405; carbonic acid, 61, 404, 405 ; hydrogen, 41, 61, 405 ; hydrogen sulphid, 61, 405 ; marsh,' 405 ; methyl mercaptan, 6 1 ; ni- trogen, 405, 41 1 ; oxygen, 405; “ stomach,” 151, 404 Gastralgia: description, 798; causation, 799 > types, 801, 802; symp- tomatology, 802 ; diagnosis, 803 ; differential diagnosis, 587 ; treatment, 805 ; idio- pathic, 801 ; secondary, 802 Gastralgokenosis, 806 Gastrectasia (see Dilation, Gastric) Gastrectomy, 361 Gastric crises, 757 ; diseases, influence upon other organs and metabolism, 374 ; douche, 299 ; idiosyncrasies, LIST OF SUBJECTS. 893 797 ; juice, physiology, 22, 47, 52; stimulation, 148; chemical examination, 156; periodic atypi- cal flow of, 834 ; chronic continu- ous flow, 857 ; absence of secre- tion, 850 Gastritis : definition and classification of, 414; acida, 458; dietetics, 194; anacida, 458 ; atrophicans, 459 ; state of blood, 403 ; diet, 232 ; mucosa or mucipara, 459 ; poly- posa, 445 ; syphilitic, 597 ; sclerosing, 613 ; stenosing, 614 acute, simple : nature and con- cept, 416; etiol- ogy, 419; path- ological histol ogy, 422 ; symp- tomatology and course, 425 ; di- agnosis, 427 ; prognosis and treatment, 428, 429 ; condition of the blood, 403 infectious : gastritis infectiosa, 438 ; diphtheritica, 438 ; mycotica, 439 ; parasitaria, 439 venenata, 441 phlegmonous or purulent, 434 chronic : concept and types, 443 ; etiology, 445 ; pathological anatomy, 447 ; symptomatology, 453 ; complications, 461 ; atypical forms, 462 ; diagnosis, 462 ; prognosis, 464 ; differ- ential diagnosis, 587 ; treatment, 231, 232, 465 ; blood changes in, 403 Gastro-anastomosis, 365 Gastrocolic ligament, 41 Gastrodiaphany of Einhorn, 104 ; as an aid to diagnosis, III Gastrodynia (see Gastralgia) Gastro-enterostomy, 361, 362 Gastro-epiploic arteries, 30 Gastro-gastrostomy, 365 Gastrograph of Einhcrn, 77; of Hemme- ter, 77, 79-81, 89 Gastroliths, 61 1 Gastrolysis, 351 Gastromalacia, 487 Gastropexy, 365 Gastroplasty, 365 Gastroptosis : observation on, 697; symp- tomatology, 723; diagnosis, 107, 108, 640, 641, 725 ; treatment, 726 Gastrorrhagia (see Hemorrhage from the Stomach) Gastrorrhaphy, 353 Gastrorrhexis, 635 Gastroscope, 179 Gastroscopy, 178 Gastrospasm, 748 Gastrostomy, 352 Gastrosuccorrhea periodica, 834 ; chronica, 837 Gastroiomy, 352 Gastroxie, 834 Gastroxynsis, 834 Gelatin, 47, 57, 60; peptones, 47, 57 Gelatoses, 57 Glands: agrtiinate, 36, 38 ; Brunner’s, 36; crypts of Lieberkiihn, 36; gastric follicles, 21, 22 ; lymph-follicles, 36, 37; mucous, 21 ; peptic, 22, 23, 27; Peyer’s patches, 36, 38; pyloric, 27, 37 ; salivary, 45 ; solitary, 36, 38 Glenard’s disease, 613 Globulin, 57 Glucosids, 42 Glycerin, 56, 61 Gmelin’s test, 132 Gout and gastric disease, 391 Granulomatous infections, 590 Guaiacum test, 133 Gymnastics, abdominal, 726 H. Heart : disturbances induced by gastric diseases, 375 ; cardiac diseases affecting the stomach, 389 Hehner-Seeman method of analysis, 170 Hemialbumoses (see Propeptone) Hemipeptone, 58 Hemoglobin, 402 Hemorrhage from the stomach, 682 ; eti- ology, 682-688 ; pathology, 688 ; symptomatology, 688 ; diagnosis, 691 ; prognosis, 694 ; treatment, 694 Hepatocolic ligament, 40 Hepatoptosis, 724 Heterochylia, 870 Heteroproteose, 49 Hour-glass stomach, 510, 643 Hunger, anomalies of the sensation of, 806 Hydrochloric acid: source, 22-24, 27, 28, 47, 48; derivation, 28, 48 ; action, 28, 47, 48, 49, 332 ; demon- stration, 50 ; in gastric antisepsis, 63, 128; interaction among se- cretions in the intes- tines, 65, 66 ; tests for HC 1 , free, 157; tests for combined, 159 ; combining capacity of 894 LIST OF SUBJECTS. foods with , 248 ; effect of alcohol on pepsin- hydrochloric acid digestion, 290 ; as medicinal agent, 328 ; in neoplasms, 550; in hypersecre- tion, 840 Hydrogen, 41, 61 Hydronephrosis, 720 Hydrotherapy, 307 Hyperacidity: true index of, 124; defini- tion and types, 196-198 ; factor in bulimia, 190 ; dietetics, 195-198, 246, 248 ; combining power of various foods with HC 1 , 248 ; relation to indican- uria, 333 ; factor in ulcer, 491 ; the clinic of, charac- teristics, 817 ; etiology, 822 ; nature and concept, 820 ; symptomatology, 823 ; prognosis, 826 ; diagnosis, 827 ; differential diagnosis, 587 ; therapeutics, 828 Hyperchlorhydria (see Hyperacidity) Hyperchylia (see Hyperacidity) Hyperesthesia, 794 ; dietetics, 207 Hypermotility as factor in bulimia, 190; the clinic of, 748 Hyperorexia (see Bulimia) Hyperperistalsis, 748 Hyperplasia, inflammatory, 447 Hypersecretion, chronic, 837 ; dietetics, 194, 247, 248 Hypochlorhydria, 847 Hypochylia, 847 I. Icterus, catarrhal, analysis of stomach con- tents in, 390 Idiopathic gastralgia, 801 Idiosyncrasies, gastric, 797 Ileodiaphany, 105 Ileum, 40 Inacidity, nervous, 850 Incontinence of the cardia, 764 ; pylorus, 771 Indican, 62, 197, 332 Indicanuria, 332 Indicators, 152, 154 Indol, 57, 61, 333 Inflammation of the stomach, suppurative (see Gastritis, Phlegmonous) Innutritious materials in food substances, 41, 42 Insufficiency of the cardia, 764 ; of the py- lorus, 771 ; of the stomach, mechanical, 774 ; motor, 624 Intestinal digestion, 52-70, 128, 826 ; fer- mentation, 61. 62, 66, 67, 128; putrefaction, 60, 62, 67, 128 Intestine : anatomy of small, 31-41 ; of large, 40 ; duodenal intubation of Hemmeter, 52-55 ; entero- diaphany, 105 ; autointoxica- tion and disinfection, 64 Intragastric stomach-shaped bag of Hem- meter, 52-55 Inulin, 56 Iron, 42, 134 Ischochymia, 651 J- Jejunum, 31, 40 K. Karyokinesis in neoplasms, 527 Kerkring, valves of, 33 Kidneys : diseases of, and the state of the stomach, 392 ; dislocation, in gastroptosis and enteroptosis, 710 ; floating and movable, 71 2 ; etiology of, 696 ; palpation, bi- manual, 714; diagnosis of pal- pable, movable, and dislocated kidney, 720 ; treatment, 727 L. Lacteals, 32, 34 Lactic acid: intestinal fermentation, 61 ; bacterial gastric product, 130 ; origin, significance, and detection, 160; quanti- tative estimation, 168, 169 ; diagnostic value in cancer, 564 ; conditions necessary ior excessive formation of, 695 Laparotomy, exploratory, 357 Lavage: double-cut rent stomach-tube, 114- 1 1 7 ; contraindications, 118, 1 19; in dilation, 202,203; i n ‘ dications for, etc., 297 Leo’s method of analysis of stomach acids, 167 Leucin, 58, 61 Leukocytosis, 401 Levulose, 48 Ligamenta coli, 41 Lipoma, 608 Literature: on gastrodiaphany, 112; on the history and technics of the stomach-tube, 125 ; exfolia- tions and erosions of gastric mucosa, 138 ; correlation of dis- eases of the stomach to those of other organs, 399 ; acute and chronic gastritis, 478 ; LIST OF SUBJECTS. phlegmonous gastritis, 482 ; ulcer, 517; carcinoma, 577; gastric tuberculosis, 595 ; gas- tric syphilis, 605 ; hypertrophic stenosis of the pylorus, 623 ; congenital hypertrophic ste- nosis of the pylorus in infants, 663 ; dilation, 675 ; gastro- ptosis and enteroptosis, 730 ; neuroses, 786 ; chronic gas- trosuccorrhea, 845 Liver, observations on dislocation of, 699 Liver-diseases and the stomach, 390 Lumbago, 724 Lymphadenoma, 609 Lymphangioma, 610 Lymphatics of stomach, 29, 30; of intes- tines, 32, 34, 38 Lymph-corpuscles, ameboid, 36 Lymphoid tissue, 34, 36 M. Macrocytes, 5 1 1 Magnesium, 42 Malaria, 385 Malformation of the gastric cavity, 591 Maltose, 44-47, 56, 65 Martius and Liittke’s method of analysis of stomach acids, 166 Massage, 309-3 11 ; and medicated irriga- tion, technic of, 312 Materia medica, 185 et seq., 328 Medicinal agents, important: HC1, 328; alkalies, 334 ; bitter tonics, 338 ; digestive ferments, 342 Megalogastria, 624, 641 Meissner, plexus of, 34, 38 Melena in carcinoma, 560, 566 Merycism, 767 Mesenteric plexus, 38 Metabolism, 35, 374 Microcytes, 511 Miliary tuberculosis, 591 Mineral springs, 313; substances of food, 42 Mitosis in gastric tumors, 562 Monobutyrin, 57 Morgagni, columns of, 41 Mosquera beef meal, 199-201 Motor function (see Peristalsis); insuffi- ciency, 624 Mouth, nose, pharynx, and larynx, effects of diseases of, on the stomach, 387 Mucigen, 35 Mucin, 60 Mucosa : structure of gastric, 21-31 ; intes- tinal, 32-38, 40 ; fragments of, in wash-water and vomit, 135- 138; diagnostic significance of exfoliations and erosions, 139 ; 895 conductivity with reference to electricity, 79-82, 304, 305 Mucous membrane (see Mucosa) Mucus, 21, 23, 25, 131 Muscular coat of stomach, 20, 28 ; of in- testine, 32 Muscularis mucosa:, 22, 32, 35 Myasthenia, gastric (see Atony, Gastric) Myoma, 609 Myxoma, 613 N. Neoplasms: benign tumors, 606; granu- lomatous infections, 590; malignant tumors, 527 Nephritis (see Kidney, Diseases) Nephroptosis (see Kidneys, Dislocation of the) Nerves of the stomach, 31 ; intestine, 32, 34, 38 Nervous diseases and the stomach, 385 ; eructation, 754 ; system and dis- eases of the stomach, 376 ; vom- iting, 756 Nessler’s reagent, 162 Neurasthenia gastrica (see Dyspepsia, Nervous) Neuroses : gastric, classification of, 733 ; dietetics of, 207, 249 ; general consideration of, 734 et seq. ; motor, 739; secretory, 817; sensory, 794 Nitrogen, 41, 41 1 Nutrition in gastric diseases, 374 O. Obturator, 183 Oligocythemia, 400 Oliguria, 723 Oppler-Boas bacillus, 129, 130, 564 Organic acids, free, 48 ; total, analysis of, 170 Orthopedic treatment, 307 P. Palpation, 98 Pancreas, 55 Pancreatic digestion, 55-57, 292 ; secre- tion, physiological stimulants of, 58 Pancreatin, 344 Papain, 346 Papayotin, 346 Papillomata, 606 Papoid, 346 Parasites, animal, and gastritis, 440 Pepsin: source and origin, 22, 24, 27, 28, 172; action, 47, 49, 172, 175; tests, 50, 172, 175 ; nature, 175 ; in the duodenum, 65 ; ultimate 896 LIST OF SUBJECTS. fate of, 68; bile action on, 60; action of alcohol on pepsin-hy- drochloric acid, 290; as a me- dicinal agent, 344 Pepsinogen (see Proenzymes) Peptone : peptic product, 49 ; test, 50 ; tryptic product, 58 ; bacterial product, 61 ; absorption of, 65 ; in the stools, 69 ; diet, 199 Peptones: casein, 57; elastin, 47, 57; gelatin, 47, 57 Peptonuria, 412 Percussion, 98 Peristalsis : influence of HC 1 , 47, 7^ ; bile influence, 60 ; comparative im- portance, 70, 90; tests, 71-90; function of, 74 ; phases, 76, 83, 84 ; passive movements, 78 ; theories relating to the move- ments of the gastric ingesta, 84-89 ; study of, by X-rays, 87; conclusions concerning physi- ology of, 89 ; electrical stimula- tion, 79-82 ; intragastric pres- sure, 89 ; factor in the patho- logical propagation of micro- organisms, 128; relation to digestibility of food substances, 186, 189 ; antiperistalsis, 2 1 2, 213 ; influence of alcohol, 293 ; neuroses of, 739 ; intestinal peristalsis, 32 Peristaltic unrest, 748 Peritonitis, perforation, 510 Pexine (see Rennin) Phenol, 61 Phloroglucin, vanillin test, 158 Phosphates, 48, 409 Phosphorus, 41, 42 Phthisis ventriculi, 850 Phytobezoar, 613 Pineapple ferments, 347 Pneumatosis, 755 Pneumogastric nerves, 31 Poikilocytosis, 402, 511 Polypi, 606 Proenzymes, pepsinogen : source, 23, 24, 27, 173; con- version into pep- sin, 27, 47, 49, 172 ; test, 173 rennin-zymogen : source, 23, 24 ; corrver- sion into rennin, 47, 174; tests, 5 L 175 Prolapsus of the stomach (see Gastropto- sis) ; colon (see Coloptosis) ; spleen (see Splenoptosis) ; liver (see Hepatoptosis) Propepsin (see Pepsinogen under Pro- enzymes) Propeptone', 49, 50 Proteids : their office in the economy, 42 ; digestion, peptic, 47, 49, 175 ; tryptic, 57, 58; proteid and bile interaction, 60 ; intestinal putre- faction, 61 ; in hyperacidity, 194-198, 249, 824 Proteolysis: peptic, 47-51, 175; tryptic, 57, 58; in hyperacidity, 194- 199, 248, 824 Proteoses, 49 Protoproteose, 49 Prozymogen, 25, 26 Ptyalin : salivary digestion, 44, 45, 1 7 1 ; of the succus entericus, 60 ; in- fluence of alcohol on, 293 ; an artificial ferment, 342 Pulmonary diseases and the stomach, 387 Pus in gastric contents, 1 33 Putrefaction: bile action, 60; products, etc., 61, 66, 67; economic relation, 62 ; promoting and inhibitory agencies, 60, 67, 68, 128; conjugate sulphates and indol, indices of, 332 Pylorectomy, 354 et seq. ; atypical, 360; partial, 360 Pyloric ligaments, 18, 20; spasm, 746; valve, 18, 20 Pyloroplasty, 363, 373 Pylorospasm, 746 Pylorus: hypertrophic stenosis of, 613; symptomatology, 618 ; diagnosis, 620 ; prognosis, 621 ; treatment, 622 insufficiency of, 771 ; obstruction of, 657 ; symptomat- ology, 658 resection of the, 354; spasm of the, 746 Pyopneumothorax subphrenicus, 510 R. Rectum, 41 Reflex vomiting, 756, 760 Regurgitation, 765 Renal diseases (see Kidney, Diseases) Rennin: source and derivation* 22, 24, 174; action, 51, 1 74; action destroyed, 66; test, 56, 174; zymogen (see Proenzymes) Resection of the pylorus, 354; statistics, 370-373 Resorcin test, 159 Resorption (see Absorption) Respiration in stomach diseases, 376 Rest and exercise, therapy of, 282-287 : cure, Weir Mitchell’s, 816 Rheumatism and gastric disease, 391 LIST OF SUBJECTS. 897 Rontgen-ray photography of stomach, 641 ; in studying peristalsis, 87 Rugae, 21 Rumination, 767 S. Saliva: detection in gastric contents, 1 3 1 ; nature and action, 44, 45, 1 7 1 ; influence of alcohol, 293 Sarcinae, 129, 439 Sarcomata, 546 ; classification and etiology, 546, 547 ; symptomatology, 547; diagnosis, 552; prog- nosis, 577 Scirrhus, gastric, 533 Secretion or secretions : physiological ex- citants of gastric and pancreatic, 58 ; contempora- neous action of, 65 ; admixtures of, 65 ; of water by the stomach, 65 ; duodenal, 66, 132; in the fasting stomach, 148 ; depend- ence on peristal- sis, 70, 90 ; con- ditioning bacte- rial propagation, 128; factor in digestibility of foods, 186, 194; in neoplasms, 550 ; neuroses of, 817 Self-digestion of the stomach, 487 Semilunar ganglion, 38 Sensation, neuroses of, 794 Sensations of hunger and of appetite, anomalies of, 800 Serous coat of intestines, 31 Sigmoid flexure, 40 Skatol, 61 Skin-diseases and digestive troubles, 396 Sodium, 42 Solar plexus, 31 Solutions, standard and normal, 152 Spasm, pyloric, 746 Spectroscopic examination, 135 Sphincter: anal, 42 ; pyloric, 20 Splanchnoptosis, 707 Splenoptosis, 724 Spray, intragastric, 300 Starches, 44-47, 58 Steapsin, 56, 60 Stenosis : cardiac, 652 ; etiology, 653 ; symptomatology, 654 ; diagnosis, 654; progno- sis, 655 ; treatment, 655 hyperplastic pyloric, 444 cicatricial pyloric, 510 hypertrophic pyloric, 613 ; symptomatology, 618 ; diagnosis, 620 ; prog- nosis, 621 ; treatment, 622 congenital pyloric, 660; diagno- sis, 662; prognosis, 663 ; treatment, 663 effects of various forms of, 664- 675 ; relative value of diagnostic factors, 660- 670 ; continued superse- cretion in, 671 degree of obstruction, 673 ; prognosis, 673 ; treatment, 673- 675 ; diet in, 651 Stomach: macroscopic anatomy, 17-21 ; histology, 20-31 ; location, size, and capacity — methods for determining these, 98-112; contents, examination, 114- 138, 141 ; acidity in the healthy and dyspeptic, 713 ; influence of its diseases upon other or- gans and metabolism, 374; in- fluence of other affections on the, 385 ; the blood and urine in gastric diseases, 400 ; gases, 15 1 , 404; the clinic, 414 et seq. ; hour-glass, 481, 591 ; hemorrhage from, 682 Stomachic remedies, 338 Stomach-pump, 123 Stomach-tube and technics of its introduc- tion, 1 14-125 Subacidity — dietetics, 189 ; clinical, 847 Submucosa of stomach, 21 ; of intestine, 3 2 Succus entericus, 60, 66, 69 Sugar, 44, 45, 59 Sugars : cane, 48, 56, 65 ; grape, 56, 65 ; invert, 48, 56 ; milk-, 65 Sulphates, 63, 332 Sulphur, 41, 42 Superacidity (see Hyperacidity) Supersecretion (see Hypersecretion) Surgery, gastric : historical review, 348 ; forms of operations, 351 ; fundamental factors in mortality, resulting, 366 Syntonin, 49, 65 Syphilis of the stomach, 596 T. Telangiectatic carcinoma, 527 Test-meals, 121-125 Tetanus, 379 Tetany, 379 Therapy of stomach diseases : dietetics, 185 ; lavage and the gastric douche, LIST OF SUBJECTS. 297 ; electricity, 301 ; hydrotherapeutic and orthopedic methods, 307 ; massage, 309 ; mineral springs, 313 ; important medicinal agents, 328 Titration, 152 Tonics, bitter, 338 Topfer’s method in analysis, 163, 164 Tormina ventriculi nervosa, 748 Transillumination (see Diaphany) Trypsin, 57, 58, 66, 68, 69, 70 Tryptones, 58 Tryptophan, 58 Tuberculosis of the stomach, 590; diagno- sis, 594 Tube, stomach-, and technics of its intro- duction, 114-126 Tumors: benign, 606; malignant, 527 ; of colon, 557; of gall-bladder, 557; of liver, 556 ; of omen- tum, 557 ; of peritoneum, 557 ; splenic, 556 Tyrosin, 58, 61 U. Ulcer of the stomach : condition of the blood in, 403 ; nature of, 486 ; self-digestion of stomach, 487 ; etiology, 489 - 49 1; symptoma- tology, 497, 547 ; diagnosis, 507- 511 ; differential diagnosis, 587 ; 587; treatment, 195, 205, 241- 243, 5 1 1 ; car- cinomatous, 108, 195 * 5o6, 559 , 570; syphilitic, 600 ; tubercular, 592 Ulcus ventriculi, pepticum, rotundum, per- forans, rodens, corrosivum e diges- tione, 486 ; carcinomatosum (see Ulcer, Carcinomatous) Urea, 394, 41 1 Urine : in gastric diseases, 406 ; acidity in the healthy and dyspeptic, 820 V. Vagus nerve, 58 Valvulae conniventes, 33 Vasa brevia, 30 Vermiform appendix, 40 Vertigo, gastric, 377 ; intestinal, 378 Vigoral, 200 Villi, 33, 34 Viscera, reversal of their location, 723 Vomiting : cerebral, central, spinal, 757 ; in pregnancy, 737 ; juvenile, 656; nervous habitual, 756; neurasthenic, hysteric, 759 ; periodical, 758 ; reflex, 756, 760 W. Water : in the animal economy, 42 ; secre- tion and absorption in the stomach, 65 Waters: natural mineral, virtues of, 313; alkaline, 317, 319; alkaline sul- phur, 318 ; chalybeate, 325, 326 ; acidulous, 327, 328 ; saline, 319, 321 ; sodium chlorid, 319 ; bitter or purgative, 321, 322 ; sulphur- etted, 323, 325 Y. Yeast fungus, 129, 439 Z. Zymogen granules, 26 Zymogens (see Proenzymes) Catalogue of the Medical, Dental, Phar- maceutical, Chemical, and Scientific Books Published by P. Blakiston’s Son & Co., 1012 Walnut Street, Philadelphia. Established 1843. SPECIAL NOTE. The prices as given in this catalogue are absolutely net — no discount will be allowed retail purchasers under any consideration. This rule has been established in order that every one will be treated alike, a general reduction in former prices having been made to meet previous retail discounts. Upon receipt of the adver- tised price any book will be forwarded by mail or express, all charges prepaid. 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Edited by Solomon Solis Cohen, a.m., m.d., Professor of Medicine and Therapeutics in the Philadelphia Polyclinic ; Lecturer on Clinical Medicine at Jefferson Medical College ; Physician to the Philadelphia and Rush Hos- pitals ; formerly Lecturer on Therapeutics, Dartmouth Medical College. To be issued in Eleven Compact Octavo Volumes. Price for Set Complete, Cloth, $22.00 Electrotherapy. Illustrated. Two Volumes. By George W. Jacoby, m.d., New York, Consulting Neurologist to the German Hospital, to the Infirmary for Women and Children, to the Craig Colony for Epileptics, etc. Special articles by Edward Jackson, a.m., m.d., Denver, Col. ; Emeritus Professor of Diseases of the Eye in the Philadelphia Polyclinic ; Member American Ophthalmological Society ; Fellow and ex-President American Academy of Medicine, etc. — By William Scheppegrell, m.d., New Orleans, Member American Laryngological, Rhinological, and Otological Society. — By J. 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(Lond.), Physician to the German Hospital, Dalston ; Assistant Physician North London Hospital for Consump- tion ; Author of “The Mineral Waters and Health Resorts of Europe and Guy Hinsdale, a.m., m.d., Secretary of the American Climatological Associa- tion ; President of the Pennsylvania Society for the Prevention of Tuberculosis ; formerly Lecturer on Medical Climatology in the University of Pennsylvania, etc. Prophylaxis — Personal Hygiene — Care of the Sick. Illustrated. By Harold C. Ernst, m.d., Professor of Bacteriology in the Medical School of Harvard University, Boston ; and Albert Abrams, m.d. (University of Heidel- berg), formerly Professor of Pathology, Cooper Medical College, San Francisco. Dietotherapy. Food in Health and Disease. By Nathan S. 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By Joseph McFarland, m.d., Professor of Pathology in the Medico-Chirurgical College, Philadelphia ; Pathologist to the Medico-Chirurgical Hospital and to the Rush Hospital for Consumptives and Allied Diseases, etc. — O. T. Osborne, m.d., Professor of Materia Medica and Therapeutics, Medical Department, Yale University, New Haven. — Frederick A. Packard, m.d., Visiting Physician to the Pennsylvania and to the Children’s Hospitals. — The Editor, and Augustus A. Eshner, m.d., Professor of Clinical Medicine in the Philadelphia Polyclinic ; Physician to the Philadelphia Hospital, etc. *** Complete descriptive circular upon application. MEDICAL AND SCIENTIFIC PUBLICATIONS. 11 Cohen. The Throat and Voice. By J. Solis Cohen, m.d. Illustrated. i2mo. Cloth, .40 Congdon. Laboratory Instructions in General Chemistry. By Ernest A. Congdon, Professor of Chemistry in the Drexel Institute, Philadelphia ; Member American Chemical Society ; Fellow of the London Chemical Society, etc. With an Appendix, useful Tables, and 56 Illustrations. Interleaved, Cloth, $1.00 Conn. Agricultural Bacteriology. Including a Study of Bacteria as Relating to Agriculture, with Special Reference to the Bacteria in Soil, in the Dairy, in Food Products, in Domestic Animals, and in Sewage. By H. W. Conn, Ph.d., Professor of Biology, Wesleyan University, Middletown, Conn.; Author of “Evolution of To-day,” “ The Story of Germ Life,” etc. With Illustrations. In Press. Cooper. Syphilis. Colored Plate. By Alfred Cooper, f.r.c.s., Senior Surgeon to St. Mark’s Hospital ; late Surgeon to the London Lock Hospital, etc. Second Edition, Edited by Edward Cot- terell, f.r.c.s., Surgeon London Lock Hospital, etc. 20 Full-page Plates contain- ing many Colored Figures. Octavo. Cloth, $5.00 Coplin. Manual of Pathology. Third Edition. 330 Illustrations. 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Half Morocco, Gilt, $1.25 Da Costa. Clinical Pathology of the Blood. Colored Plates. A Practical Guide to the Examination of the Blood by Clinical Methods, with Refer- ence to the Diagnosis of Disease. By John C. Da Costa, Jr., m.d., Assistant Demonstrator of Clinical Medicine in the Jefferson Medical College, Philadelphia ; Assistant in the Medical Clinic, Jefferson Medical College Hospital ; Haematologist to the German Hospital. With six Colored Plates and other Illustrations. Octavo. In Press. Deaver. Surgical Anatomy. 400 Full-page Plates. A Treatise on Human Anatomy in its Application to the Practice of Medicine and Surgery. By John B. Deaver, m.d., Surgeon-in-Chief to the German Hospital ; Surgeon to the Children’s Hospital and to the Philadelphia Hospital; Consulting Surgeon to St. Agnes’, St. Timothy’s, and Germantown Hospitals ; formerly Assistant Professor of Applied Anatomy, University of Pennsylvania, etc. With over 400 very handsome Full-page Illustrations engraved from original drawings made by special artists from dissections prepared for the purpose in the dissecting-rooms of the University of Pennsylvania. Three large volumes. Royal square octavo. Sold by Subscription. Orders taken for complete sets only. Description upon Application. Cloth, $21.00 ; Half Morocco or Sheep, $24.00; Half Russia, $27.00 Synopsis of Contents. Volume I. — Upper Extremity — Back of Neck, Shoulder, and Trunk — Cranium — Scalp — Face. Volume II. — Neck — Mouth, Pharynx, Larynx, Nose — Orbit — Eyeball — Organ of Hearing — Brain — Female Perineum — Male Perineum. Volume III. — Abdominal Wall — Abdominal Cavity — Pelvic Cavity — Chest — Lower Extremity. ‘ ‘ In summing up the general excellences of this remarkable work, we can accord our unqual- ifiedfpraise for the accurate, exhaustive, and systematic manner in which the author has carried out his plan, and we can commend it as a model of its kind, which must be possessed to be appre- ciated.” — The Medical Record , New York. Appendicitis. Second Edition. Its History, Anatomy, Etiology, Pathology, Symptoms, Diagnosis, Prognosis, Treatment, Complications, and Sequelae. A Systematic Treatise, with 22 Plates, 10 of which are Colored, drawn specially for this work. Second Edition, Re- vised and Rewritten. 8vo. Just Ready. Cloth, $3.50 MEDICAL AND SCIENTIFIC PUBLICATIONS. 13 Dercum. Rest — Mental Therapeutics — Suggestion. See Cohen, Physiologic Therapeutics, page io. Duckworth. On Gout. Illustrated. A Treatise on Gout. By Sir Dyce Duckworth, m.d. (Edin.), f.r.c.p., Physician to, and Lecturer on Clinical Medicine at, St. Bartholomew’s Hospital, London. With Chromo-lithographs and Engravings. Octavo. Cloth, $6.00 Diihrssen. A Manual of Gynecological Practice. By Dr. A. Duhrssen, Privat-Docent in Midwifery and Gynecology in the University of Berlin. Translated from the Fourth German Edition and Edited by John W. Taylor, f.r.c.s., Surgeon to the Birmingham and Midlands Hospital for Women ; Vice-President of the British Gynecological Society; and Frederick Edge, m.d., m.r.c.p., f.r.c.s., Surgeon to the Wolverhampton and District Hospital for Women. With 105 Illustrations. i2mo. Cloth, $1.50 Dulles. What to Do First In Accidents and Poisoning. By C. W. Dulles, m.d., Surgeon to the Rush Hospital ; formerly Assistant Surgeon 2d Regiment N. G. Pa., etc. Fifth Edition, Enlarged. With new Illustrations. i2mo. Cloth, $1.00 Edgar. Text-Book of Obstetrics. By J. 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Hale, m.d., Ophthalmic Surgeon United Hebrew Charities ; Consulting Ophthalmic Surgeon Charity Hospital, Chicago ; late Vol. Assistant Imperial Eye Clinic, University of Kiel. With a Glossary and 158 Illustrations, many of which are in Colors. 8vo. Cloth, $4.50; Sheep, $5.50; Half Russia, $6.50 Fillebrown. A Text-Book of Operative Dentistry. Written by invitation of the National Association of Dental Faculties. By Thomas Fillebrown, m.d., d.m.d., Professor of Operative Dentistry in the Dental School of Harvard University ; Member of the American Dental Association, etc. Illustrated. 8vo. Cloth, $2.25 14 P. BLAKISTON' S SON 6 - CO.'S Fowler’s Dictionary of Practical Medicine. By Various Writers. An Encyclopedia of Medicine. Edited by James Kingston Fowler, m.a., m.d., f.r.c.p., Senior Assistant Physician to, and Lecturer on Patho- logical Anatomy at, the Middlesex Hospital, London. 8vo. Cloth, $3.00 ; Half Morocco, $4.00 Fullerton. Obstetric Nursing. By Anna M. 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Illustra- ted with Charts, Diagrams, and Full-page Plates. Cloth, $3.00 Gould. The Illustrated Dictionary of Medicine, Biology, and Allied Sciences. Fifth Edition." Being an Exhaustive Lexicon of Medicine and those Sciences Collateral to it : Biology (Zoology and Botany), Chemistry, Dentistry, Pharmacology, Microscopy, etc. By George M. Gould, a.m., m.d., Editor of American Medicine ; President, 1 893-94, American Academy of Medicine, etc. With many Useful Tables and numer-' ous Fine Illustrations. Large Square Octavo. 1633 pages. Fifth Edition. Just Ready. Full Sheep or Half Dark-Green Leather, $10.00 With Thumb Index, $11.00 ; Half Russia, Thumb Index, $12.00 “Few persons read dictionaries as Theophile Gautier did — for pleasure; if, however, all dictionaries were as readable as the one under consideration, his taste for this kind of literature would be less singular. . . . The book is excellently printed, and the illustrations are admir- ably executed. The binding is substantial and even handsome, but the business-like ‘ get-up ’ of the book makes it well fitted for use as well as for the adornment of a book-shelf.’ ’ — The British Medical Journal , London. The Student’s Medical Dictionary. Eleventh Ed. Illustrated. Enlarged. Including all the Words and Phrases generally used in Medicine, with their proper Pronunciations and Definitions, based on Recent Medical Literature. With Tables of the Bacilli, Micrococci, Leukomains, Ptomains, etc., of the Arteries, Muscles, Nerves, Ganglia, and Plexuses; Mineral Springs of the U. S., etc., and a new Table of Eponymic Terms and Tests. Rewritten, Enlarged, and Improved. With many Illustrations. Small octavo. 840 pages. Half Morocco, $2.50; Thumb Index, $3.00 “ One pleasing feature of the book is that the reader can almost invariably find the definition under the word he looks for, without being referred from one place to another, as is too commonly the case in medical dictionaries. The tables of the bacilli, micrococci, leukomains, and ptomains are excellent, and contain a large amount of information in a limited space. The anatomical tables are also concise and clear. . . .We should unhesitatingly recommend this dictionary to our readers, feeling sure that it will prove of much value to them.” — The American Journal of Medical Science. MEDICAL AND SCIENTIFIC PUBLICATIONS. 15 Gould. The Pocket Pronouncing Medical Lexicon. Fourth Edition. (30,000 Medical Words Pronounced and Defined.) A Student’s Pronouncing Medical Lexicon. Containing all the Words, their Defini- tions and Pronunciations, that the Student generally comes in contact with ; also elaborate Tables of the Arteries, Muscles, Nerves, Bacilli, etc., etc.; a Dose List in both English and Metric Systems, a new table of Clinical Eponymic Terms, etc., arranged in a most convenient form for reference and memorizing. Thin 64010. (6 x 3^ inches.) 838 pages. The System of Pronunciation used in this book is very simple. A New Edition. Full Limp Leather, Gilt Edges, $1.00 ; Thumb Index, $1.25 “ This ‘ Dictionary ’ is admirably suited to the uses of the lecture-room, or for the purposes of a medical defining vocabulary — many of the words not yet being found in any other dictionary, large or small, while all of the words are those of the living medical literature of the day.” — The Virginia Medical Monthly. *** 120,000 copies of Gould’s Dictionaries have been sold. Sample pages and descriptive circulars of Gould' s Dictionaries free upon application. Borderland Studies. Miscellaneous Addresses and Essays Pertaining to Medicine and the Medical Profession, and their Relations to General Science. 350 pages. i2mo. Cloth, $2.00 Gould and Pyle. Cyclopedia of Practical Medicine and Surgery. 72 Special Contributors. Illustrated. One Volume. A Concise Reference Handbook, Alphabetically Arranged, of Medicine, Surgery, Obstetrics, Materia Medica, Therapeutics, and the various specialties, with Particular Reference to Diagnosis and Treatment. Compiled under the Editorial Supervision of Drs. George M. Gould and W. L. Pyle. With many Illustrations. Large Square 8vo. To correspond with Gould’s “Illustrated Dictionary.” Full Sheep or Half Dark-Green Leather, $10.00 ; With Thumb Index, $11.00 Half Russia, Thumb Index, $12.00 *** The great success of Dr. Gould’s “Illustrated Dictionary of Medicine” sug- gested the preparation of this companion volume, which should be to the physician the same trustworthy handbook in the broad field of general information that the Dictionary is in the more special one of the explanation of words and the statement of facts. The aim has been to provide in a one-volume book all the material usually contained in the large systems and much which they do not contain. Instead of long, discursive papers on special subjects there are short, concise, pithy articles alphabetically arranged, giv- ing the latest methods of diagnosis, treatment, and operating — a working book in which the editors and their collaborators have condensed all that is essential from a vast amount of literature and personal experience. The seventy-two special contributors have been selected from all parts of the country in accordance with their fitness for treating special subjects about which they may be considered expert authorities. They are all men of prominence, teachers, investigators, and writers of experience, who give to the book a character unequaled by any other work of the kind. At each reprinting this Cyclopedia is carefully revised and augmented so as to in- clude important innovations and in order to keep it up-to-date. “ The book is a companion volume to Gould’s ‘Illustrated Dictionary of Medicine,’ which every physician should possess. 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The authors have had large experience as Quiz-Masters and attaches of colleges, and are well acquainted with the wants of students. They are arranged in the most approved form, thorough and concise, containing about 800 illustrations, inserted wherever they could be used to advantage. Can be used by students of any college, and contain information nowhere else collected in such a condensed practical shape. ILLUSTRATED CIRCULAR FREE. No. 1. HUMAN ANATOMY. Sixth Revised and Enlarged Edition. Including Vis- ceral Anatomy. Can be used with either Morris’s or Gray’s Anatomy. 1 1 7 Illustrations and 16 Lithographic Plates of Nerves and Arteries, with Explanatory Tables, etc. By Samuel O. L. Potter, m.d., formerly Professor of the Practice of Medicine, Cooper Medical College, San Francisco; Major and Brigade Surgeon, U. S. Vol. No. 2. PRACTICE OF MEDICINE. Part I. Sixth Edition, Revised, Enlarged, and Improved. By Dan’l E. Hughes, M.d., Physician -in-Chief, Philadelphia Hospital; late Demonstrator of Clinical Medicine, Jefferson Medical College, Philadelphia. No. 3. PRACTICE OF MEDICINE. Part II. Sixth Edition, Revised, Enlarged, and Improved. Same author as No. 2. No. 4. PHYSIOLOGY. Tenth Edition, with new Illustrations. Enlarged and Revised. By A. P. Brubaker, m.d., Professor of Physiology in the Pennsylvania College of Dental Surgery; Adjunct Professor of Physiology, Jefferson Medical College, Philadelphia. No. 5. OBSTETRICS. Sixth Edition. By Henry G. Landis, m.d. Revised and Edited by Wm. H. Wells, m.d., Instructor of Obstetrics, Jefferson Medical College, Philadelphia. Enlarged. 3 Plates and 47 other Illustrations. No. 6. MATERIA MEDIC A, THERAPEUTICS, AND PRESCRIPTION WRITING. Sixth Revised Edition. Same author as No. 1. No. 7. GYNECOLOGY. Second Edition. By Wm. H. Wells, m.d., Instructor of Obstet- rics, Jefferson Medical College, Philadelphia. 140 Illustrations. No. 8. DISEASES OF THE EYE AND REFRACTION. Second Edition. Includ- ing Treatment and Surgery and a Section on Local Therapeutics. By George M. Gould, M.d., Editor Philadelphia Medical Journal, and W. L. Pyle, M.D. , Assistant Surgeon, Wills Eye Hospital. With Formulae, Glossary, several useful Tables, and 109 Illustrations. No. 9. SURGERY, Minor Surgery, and Bandaging. Fifth Edition, Enlarged and Im- proved. By Orville Horwitz, b.s., m.d., Clinical Professor of Genito-Urinary Surgery and Venereal Diseases in Jefferson Medical College ; Surgeon to Philadelphia Hospital, etc. With 98 Formulae and 167 Illustrations. No. 10. MEDICAL CHEMISTRY. Fourth Edition. Including Urinalysis, Chemistry of Milk, Blood, etc. By Henry Leffmann, m.d., Professor of Chemistry in Pennsylvania College of Dental Surgery and in the Woman’s Medical College, Philadelphia. No. 11. PHARMACY. Fifth Edition. Based upon Professor Remington’s Text-Book of Pharmacy. By F. E. Stewart, m.d., ph.g., late Quiz-Master in Pharmacy and Chemistry, Philadelphia College of Pharmacy; Lecturer at Jefferson Medical College. No. 12. VETERINARY ANATOMY AND PHYSIOLOGY. Illustrated. By Wm. R. Ballou, m.d., Professor of Equine Anatomy at New York College of Veterinary Sur- geons; Physician to Bellevue Dispensary, etc. With 29 graphic Illustrations. No. 13. DENTAL PATHOLOGY AND DENTAL MEDICINE. Third Edition, Illustrated. By George W. Warren, d.d.S., Pennsylvania College of Dental Surgery. No. 14. DISEASES OF CHILDREN. Colored Plate. By Marcus P. Hatfield, Professor of Diseases of Children, Chicago Medical College. Second Edition, Enlarged. No. 15. GENERAL PATHOLOGY. Illustrated. By A. E. Thayer, m.d., etc. Preparing. No. 16. DISEASES OF THE SXIN. By Jay F. Schamberg, m.d, Professor of Skin Diseases, "Philadelphia Polyclinic. Second Edition, Revised. 105 Illustrations. No. 17. HISTOLOGY. Illustrated. By H. H. Cushing, m.d. Preparing. 41 JUST READY, ONE VOLUME A Cyclopedia of Practical Medicine and Surgery A CONCISE REFERENCE BOOK, ALPHABETICALLY ARRANGED OF MEDICINE, SURGERY, OBSTETRICS, MATERIA MEDICA, THERAPEUTICS, AND THE VARIOUS SPECIALTIES, WITH PARTICULAR REFERENCE TO DIAGNOSIS AND TREATMENT COMPILED UNDER THE EDITORIAL SUPERVISION OF GEORGE M* GOULD, MJX AND WALTER L. PYLE, M.D. Author of ** An Illustrated Dictionary of Medicine ? ” Assistant Surgeon Wills Eye Hospital? formerly Editor ** Philadelphia Medical Journal,” etc. Editor ** International Medical Magazine,” etc. AND SEVENTY-TWO SPECIAL CONTRIBUTORS WITH MANY ILLUSTRATIONS LARGE SQUARE OCTAVO. TO CORRESPOND WITH GOULD'S “ ILLUSTRATED DICTIONARY.” FULL SHEEP OR HALF DARK-GREEN LEATHER, $10.00? WITH THUMB INDEX, $H.00? HALF RUSSIA, THUMB INDEX, $12.00, NET The great success of Dr. Gould’ s * ‘ Illustrated Dictionary of Medicine ’ * suggested the preparation of this companion volume, which should be to the physician the same trustworthy handbook in the broad field of general information that the Dictionary is in the more special one of the explanation of words and the statement of facts. The aim has been to provide in a one-volume book all the material usually contained in the large systems and much which they do not contain. Instead of long discursive papers on special subjects there are short, concise, pithy articles alphabetically arranged, giving the latest methods of diagnosis, treatment, and operating — a working book in which the editors and their collaborators have condensed all that is essential from a vast amount of literature and personal experience. The illustrations have been selected with care, only those having been used that are of practical value ; no effort has been made to overload the book with useless pictures. The seventy-two special contributors — the names of whom are given on the following page — have been selected from all parts of the country in accordance with their fitness for treating special subjects about which they may be considered expert authorities. They are all men of prominence, teachers, investigators, and writers of experience, who give to the book a character unequaled by any other work of the kind. V LARGE DESCRIPTIVE CIRCULAR UPON APPLICATION 42 GOULD AND PYLE’S CYCLOPEDIA OF MEDICINE LIST OF CONTRIBUTORS Samuel W. Abbott, A.M., M.D., Boston. James M. Anders, M.D., LL.D., Phila. Joseph D. Bryant, M.D., New York. James B. Bullitt, M.D., Louisville. Charles H. Burnett, A.M., M.D., Phila. J. Abbott Cantrell, M.D., Philadelphia. Archibald Church, M.D., Chicago. L. Pierce Clark, M.D., Sonyea, N. Y. Solomon Solis-Cohen, M.D., Philadelphia. Nathan S. Davis, Jr., M.D., Chicago. Theodore Diller, M.D., Pittsburg. Augustus A. Eshner, M.D., Philadelphia. J. T. Eskridge, M.D., Denver, Col. J. McFadden Gaston, A. B., M.D., Atlanta, Ga. J. McFadden Gaston, Jr., A.M., M.D., At- lanta, Ga. Virgil P. Gibney, M.D., New York. George M. Gould, A.M., M.D., Phila. W. A. Hardaway, A.M., M.D., St. Louis. John C. Hemmeter, M.B., M.D., Baltimore. Barton Cooke Hirst, M.D., Philadelphia. Bayard Holmes, M.D., Chicago. Orville Horwitz, B.S., M.D., Philadelphia. Daniel E. Hughes, M.D., Philadelphia. James Nevins Hyde, A.M., M.D., Chicago. E. Fletcher Ingals, A.M., M.D., Chicago. Abraham Jacobi, M.D., New York. William W. Johnston, M.D., Washington, D. C. Wyatt Johnston, M.D., Montreal. Allen A. Jones, M.D., Buffalo. William W. Keen, M.D., LL.D., Phila. Howard S. Kinne, M.D., Philadelphia. Ernest Laplace, M.D., Philadelphia. Benjamin Lee, M.D., Philadelphia. Charles L. Leonard, M.D., Philadelphia. James Hendrie Lloyd, A.M., M.D., Phila. J. W. MacDonald, M.D. (Edin.), F.R.C.S. Ed., Minneapolis. L. S. McMurtry, M.D., Louisville. G. Hudson Makuen, Philadelphia. Matthew D. Mann, M.D., Buffalo. Henry O. Marcy, A.M., M.D., LL.D., Boston. Rudolph Matas, M.D., New Orleans. Joseph M. Mathews, M.D., Louisville. John K. Mitchell, M.D., Philadelphia. Harold N. Moyer, M.D., Chicago. John H. Musser, M.D., Philadelphia. A. G. Nicholls, M.D., Montreal. A. H. Ohmann-Dusmesnil, M.D., St. Louis. William Osier, M.D., Baltimore. Samuel O. L. Potter, A.M., M.D., M.R. C.P. (London), San Francisco. Walter L. Pyle, A.M., M.D., Philadelphia. B. Alexander Randall, A.M., M.D., Phila. Joseph Ransohoff, M.D., F.R.C.S. (Eng.), Cincinnati. Jay F. Schamberg, A.M., M.D., Phila. Nicholas Senn, M.D., LL.D., Chicago. Richard Slee, M.D., Swiftwater, Pa. S. E. Solly, M.D., M.R.C.S., Colorado Springs, Col. Edmond Souchon, M.D., New Orleans. Ward F. Sprenkel, M.D., Philadelphia. Charles G. Stockton, M.D., Buffalo. John Madison Taylor, A.M., M.D., Phila. William S. Thayer, M.D., Baltimore. James Thorington, A.M., M.D., Phila. Martin B. Tinker, M.D., Philadelphia. James Tyson, M.D., Philadelphia. J. Hilton Waterman, M.D., New York. H. A. West, M.D., Galveston, Texas. J. William White, M.D., PH.D., Phila. Reynold W. Wilcox, M.A., M.D., LL.D., New York. George Wilkins, M.D., Montreal. DeForest Willard, M.D., Philadelphia. Alfred C. Wood, M.D., Philadelphia. Horatio C. Wood, M.D., LL.D., Phila. Albert Woldert, PH.G., M.D., Phila. James K. Young, M.D., Philadelphia. 43 Deaver'S Surgical Anatomy A Treatise on Human Anatomy- in its Application to the Practice of Medicine and Surgery & & By JOHN B. DEAVER, M.D. Surgeon-in- Chief to the German Hospital , Philadelphia ; Surgeon to the Children' s Hospital; Consulting Surgeon to St. Agnes', St. Timothy' s , and Germantown Hospitals; formerly Assistant Professor of Applied » Anatomy, University of Pennsylvania, etc. In Three Royal Octavo Volumes, containing about Four Hundred and Fifty Full-page Plates, nearly all from dissections made for the purpose Handsome Cloth, $21.00 ; Full Sheep, $24.00; Half Green Morocco, Marbled Edges, $24.00 ; Half Russia, Gilt, Marbled Edges, $27.00 net. SYNOPSIS OF CONTENTS VOLUME L — Upper Extremity — Back of Neck, Shoulder, and Trunk — Cranium — Scalp — Face. VOLUME IL — Neck — Mouth, Pharynx, Larynx, Nose— Orbit — Eyeball — Organ of Hearing — Brain — Female Perineum — Male Perineum. VOLUME IIL — Abdominal Wall — Abdominal Cavity — Pelvic Cavity — Chest — Lower Ex- tremity. The book is designed to aid the general practitioner and surgeon in his everyday work. The text is excellently clear, succinct, and systematically arranged, and contains a wealth of illustrations far in advance of the usual text-book. It is not intended merely for the surgeon — though to him it will prove invaluable — but for the general physician, who, while called upon to cope with innumerable emergencies and special cases, has not the means or the hospital facilities by which he can readily acquaint himself with every phase of anatomy — superficial and deep — as applied to disease and the most modern methods of treatment of injuries. To the specialist it will prove of great value. The anatomy of the head and neck, the spinal cord, the organs of sense, and the throat appeals directly to the ophthalmologist, aurist, rhinologist, laryngologist, and neurologist, while those sections devoted to the abdomen and pelvic cavity will give the gynecologist and specialist on diseases of the urinary organs, rectum, etc., material regarding the relations of the parts and the operations thereon, unique in many ways, and in a manner never before so exactly and concisely stated. To those devoted to these specialties it will prove a supplement to other text-books that omit special anatomy, and which do not attempt to show the applied anatomy* 44 Deaver’s Surgical Anatomy The illustrations, which at the first glance appear as the prominent feature of the book — but which in reality do not overshadow the text — consist of a series of pictures absolutely unique and fresh. They will bear comparison from an artistic point of view with any other work, while from a practical point of view there is no other volume or series of volumes to which they can be compared. When originally an- nounced, the book was to contain two hundred illustrations. As the work of prepara- tion progressed, this number gradually increased until it is estimated that there will now be more than four hundred full-page plates, many of which contain more than one figure. With the exception of a few minor pictures made from preparations in the possession of the author, they have all been drawn by special artists from dissections made for the purpose in the dissecting-rooms of the University of Pennsylvania. Their accuracy cannot be questioned, as each drawing has been submitted to the most careful scrutiny. From The Medical Record, New York, 44 The reader is not only taken by easy and natural stages from the more superficial to the deeper regions, but the various important regional landmarks are also indicated by schematic tracing upon the limbs* Thus the courses of arteries, veins, and nerves are indicated in a way that makes the lesson strikingly impressive and easily learned. No expense, evidently, has been spared in the preparation of the work, judging from the number of full-page plates it contains, not counting the smaller drawings. Most of these have been ‘ drawn by special artists from dissections made for the purpose in the dissecting-rooms of the University of Pennsylvania.’ In summing up the general excellences of this remarkable work, we can accord our unqualified praise for the accurate, exhaustive, and systematic manner in which the author has carried out his plan, and we can commend it as a model of its kind, which must be possessed to be appreciated.” From The Philadelphia Medical Journal. “ Many members of the profession to whom Dr. Deaver is well known either personally or by reputation as a surgeon, writer, teacher, and practical anatomist, have awaited the appearance of his Surgical Anatomy with the expectation of finding in it a guide in this difficult branch of medi- cine of much more than ordinary practical value, and their expectations will not be disappointed ♦” From The Journal of the American Medical Association. “In order to show its thoroughness, it is only necessary to mention that no less than twelve full-page plates are reproduced in order to accurately portray the surgical anatomy of the hand, and it is doubtful whether any better description exists in any work in the English language.” From The Southern California Practitioner. “ Aside from the merit of this great work, it will be a delight to the lover of books. Its gen eral make-up shows the highest development of the book-making art. The bibliophile, when holding one of these volumes in his hands, would be as careful with it as though he were handling an infant, and to drop it would cause him the keenest pain. The illustrations, the print, and the paper and binding are each and all delightful in themselves, and yet the text is concise and clear, and taken with the illustrations make a remarkably good substitute for the dissecting-room. To have these three volumes on his library shelves will be a source of pride and joy and profit to every practitioner. Dr. Deaver has in these volumes conferred a boon upon the medical profession which has, at least, never been surpassed by any one.” From The New Orleans Medical and Surgical Journal. “ While the needs of the undergraduate have been fully kept in view, it has been the aim of the author to provide a work which would be sufficient for reference for use in actual practice. We believe the book fulfils both requirements. The arrangement is systematic and the discussion erf surgical relations thorough.” Large Descriptive Circular will be sent upon application 45 Hemmeter. Diseases of the Stomach* Second Edition, Enlarged. Illustrated. Their Special Pathology, Diagnosis, and Treatment. With Sections on Anatomy, Analysis of Stomach Contents, Dietetics, Surgery of the Stomach, etc. By John C. Hemmeter, m.d., philos. d., Professor in the Medical Department of the University of Maryland ; Consultant to the University Hospital ; Director of the Clinical Laboratory, etc. Second Revised Edition. With Colored and other Illustrations. Octavo. 890 pages. Cloth, $ 6.00 ; Leather, $7.00 ; Half Russia, $8.00 *** The rapid sale of the first edition of this book has encouraged the author to revise it very thoroughly and to add much new material (about 100 pages) and a num- ber of new illustrations. About two-thirds of the book has been actually reconstructed. The section on Dietetics will be found particularly useful. “ A second enlarged and revised edition appearing in a little over a year from the date of the original publication speaks for the popularity and value of the work. This book easily occupies the first place among its sort in the English language and is particularly free from that enthusiastic hobby riding which is not unknown among gastro-enterologists. The bibliographical references are very full and complete, and the work is one of the highest order as well as one of the utmost practical value.” — Chicagp Medical Recorder. “ This edition of Hemmeter’s work on ‘ Diseases of the Stomach ’ contains much new and important material. The following articles have been added : Hypertrophic stenosis of the pylorus, obstruction of the orifices, the use and abuse of rest and exercise in the treatment of digestive dis- eases. Part of the chapter on motor insufficiency, electro-diaphany, hemorrhage from the stomach, and the articles on gastroptosis and enteroptosis have been entirely rewritten. The present edition will undoubtedly gain as many friends as the first edition. ” — The Medical Record , New York. “ Dr. Hemmeter certainly provides a book which is well worthy of a careful study. ... It treats of many subjects in an original manner, and is not only based on a considerable personal experience, but takes due notice of the labors of other well-known workers in this field.” — British Medical Journal. “ Completely scientific, modern, accurate, and creditable. . . . We commend it.” — Journal oj the American Medical Association. “We know of no work from which the physician may gain more information than this.” — Australian Medical Gazette. “ The consideration of the general methods of clinical examination of the stomach is thor- oughly adequate.” — Boston Medical and Surgical Journal. “ We part from Dr. Hemmeter’s book with the sense that it embodies the best knowledge of the time.” — London Lancet. “ We wish to express unqualified approval of the tendency which is shown to emphasize the simple and more practical methods of diagnosis.” — New York Medical Journal. “The best contemporary treatise on diseases of the stomach which we possess, not only in America, but in the whole world.’ f — Prof. L. Boas , of Berlin. In Preparation by the same Author Diseases of the Intestines. Original Illustrations A Complete, Systematic Treatise, Including the Surgical Aspects of the Subject. 46 Gordinier. The Gross and Minute Anatomy of the Central Nervous System. Colored Illustrations. By H. C. Gordinier, a.m., m.d., Professor of Physiology and of the Anatomy of the Nervous System in the Albany Medical College ; Member American Neuro- logical Association. With 48 Full-page Plates and 213 other Illustrations, a number of which are printed in Colors and many of which are original. Large 8vo. Cloth, $ 6.00 ; Sheep, $ 7.00 ; Half Russia, $8.00. *** It is universally acknowledged that for a proper comprehension of the normal and abnormal activities of an organ a thorough knowledge of its anatomy is absolutely essential. This is particularly true of diseases of the central nervous system, for in no other way can the disease symptoms be explained. Without this knowledge, clinical and pathologic observations are of little avail. This book is not a theoretic and tech- nical student’s book, but a useful working supplement to all works upon general practice and neurology, and as such is destined to mark an epoch in medical literature. “ This is an excellent book on a fascinating subject, and the author deserves the thanks of the English-speaking medical world for his labor in getting it up. There are works enough on general anatomy, and dry enough they are, as we all remember only too well ; but the anatomy of the nervous system alone is another matter entirely, for it is one of the most interesting of all subjects of medical study, at the same time that it is one of the most difficult. For both of these reasons the subject is deserving of a treatise by itself, and should not be briefly discussed in a few pages of a general work on anatomy, or in an introductory chapter of a treatise on diseases of the ner- vous system.” — Medical Record, New York. “ The author has made an honest attempt to place in the hands of the English student a comprehensive and accurate text-book, devoid of the many intricacies of modern thought and speculation. For the average man the work will appeal strongly ; the facts that he can use are readily found.” — The Journal of Nervous and Mental Diseases , New York. “ Throughout the book the descriptions of the gross and minute anatomy are, as a rule, clear, objective, and as easy of comprehension as could be expected of so difficult a subject. The state- ments are most of them quite didactically made, but this we consider an advantage rather than a defect, especially in a text-book for students as well as practitioners. . . . The chapter on cerebral localization is carefully written, and gives the most recent results on the subject.” — The American Journal of Insanity , Baltimore. “ Represents much painstaking research, and bears also the stamp of original investigation. It is unusually well written, and the illustrations, many of which are original, are well chosen. It is destined to take its place among the standard books of its class.” — New York Medical Journal. “ This book will be welcomed by teachers, practitioners, and students. It will save teachers and writers on the nervous system the necessity of accompanying their lectures and books on diseases of the nervous system with chapters on anatomy. It is really the first thoroughly system- atic work on the anatomy of the central nervous system that has appeared in the English language. The work is the more necessary because diseases of the central nervous system are becoming more and more recognized, and because the works on general anatomy do not pretend to describe the minute anatomy of the central nervous system. Authors of books on neurology recognize the fact that their readers cannot understand the descriptions of the diseases of the central nervous system without a knowledge of the anatomy of the parts involved. The subject is a difficult one at best, but the student who will make an earnest effort to master the details cannot fail to do so with the aid of this work. The author’s descriptions are clear, concise, comprehensive, and profusely and beautifully illustrated.” — Pacific Medical Journal , San Francisco. “ As there can be no accurate understanding of the diseases of the nervous system without a thorough knowledge of the anatomy, it is no wonder that the average practitioner is as ignorant of neurology as is unfortunately the case. The present volume is a praiseworthy attempt to remove the approach that has thus far rested upon English and American neurology.” — Boston Medical and Surgical Journal. “ We commend Gordinier’s chapter on cerebral localization. This will be especially helpful to clinicians, although all the views expressed in it are not yet outside of the domain of controversy. We should like to say more about Gordinier’s book, but space forbids. It is handsomely printed and copiously illustrated, and we can recommend it as a good text-book of nervous anatomy.” — Philadelphia Medical Journal. 47 JUST READY PRACTICAL GYNECOLOGY A Modern Comprehensive Text-Book By E. E. MONTGOMERY, M.D. Professor of Gynecology, Jefferson Medical College? Gynecologist to the Jefferson Medical College and St. Joseph's Hospitals? Consulting Gynecologist to the Philadelphia Lying-in Charity WITH FIVE HUNDRED AND TWENTY-SEVEN ILLUSTRATIONS Nearly all of which have been Drawn and Engraved Specially for this Work, for the most part from Original Sources OCTAVO* 819 PAGES CLOTH, $5.00 ; LEATHER, $6.00 ; HALF RUSSIA, $7.00 EXTRACT FROM THE PREFACE This work has been under consideration for the past fifteen years, and much of it has been several times rewritten. An effort has been made to make it a comprehensive work upon the subject, giving the experience and methods of the most careful men, while my own experience has been utilized to indicate that which I have found most useful and worthy of acceptance. Each general subject is considered with reference to its influence upon the entire genital tract, and the work is divided into sections rather than chapters. This course, although a departure from the ordinary text-book arrangement, is that which experience has demonstrated to be most effective in impressing the subject upon the student, and would seem to me preferable to him who uses the book to refresh his knowledge upon some particular subject. The illustrations are arranged solely with the purpose of rendering clear the text and to promote the work of diagnosis and treatment. For the excellence and character of the illustrations I am greatly indebted to the generosity of the publishers and to the skill and patience of their artists, Messrs. Shannon and Von du Lancken. To the kindly oversight of Dr. Robert L. Dickinson is due much of the exactness of the drawings. Acknowledgment is due Miss Eleanor A. Cantner for her ability in the preparation of preliminary sketches and of the index. Should it be the means of lightening the work of the student, of making more clear the pathway of the busy practitioner, and, most of all, of benefiting suffering women through improved methods of diagnosis and treatment, I shall feel well repaid for the many days and nights of labor which it has cost. 48 *