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Perforation of the colon is a rather uncommon complication of ulcerative colitis. Bargen, 1 in a series of 693 cases of ulcerative colitis with two hundred and sixty-eight complications of various types, found perforation fifth in order of frequency. Bargen and Jacobs 2 reported twenty-two perforations (3.4 per cent) in 647 cases. Jackman, Bargen and Helmholz 3 found two perforations in 95 cases of ulcerative colitis in children (2 per cent) and sixteen in the total group of 871 cases (1.1 per cent). As nearly as can be judged from the literature, free perforation of the colon with generalized peritonitis has hitherto been a fatal occurrence. Chronic perforation with abscess formation, on the other hand, is not infrequently followed by recovery. The purpose of this paper is to report 3 cases of what was considered to be perforation of the colon with generalized peritonitis successfully treated with sulfonamide drugs and

DUODENUM Congenital Anomalies. —Sumner and Morris217report a case in which duodenal atresia in a newborn infant, diagnosed early, was successfully treated by duodenojejunostomy. In Mosquera's218case the atresia proved fatal at the age of 18 months. Secretion. —Comfort219reviews the literature of the last thirty years on duodenal content in health and disease and reaches the following conclusions: During fasting the duodenal content of healthy subjects with achlorhydria is alkaline; in those with acid-secreting stomachs it is acid both in the fasting state and after meals; the reaction of the duodenal content of healthy subjects varies roughly with the amount of acid entering the duodenum; the acidity does not vary greatly between the first and the second portion; drugs, such as atropine sulfate, morphine and the sodium salt of dehydrocholic acid, increase the averagepHof the duodenal content; the antacids

Summary Hepatic function was measured in 50 patients with portal cirrhosis of the liver. Twenty healthy persons were studied similarly as a control group. The cases of portal cirrhosis were classified arbitrarily into three groups on the basis of clinical severity: I) 14 patients without symptoms, "latent" cirrhosis; II) 23 with moderate clinical symptoms of hepatic failure; and III) 13 individuals severely ill and deeply jaundiced. Marked differences were found corresponding, in general, with the clinical severity of illness. In the group without symptoms attributable to the liver per se, parenchymal function was not significantly changed when compared with the normal group, whereas markedly abnormal and significant deviations were encountered in severely ill patients with hepatic failure and deep jaundice. Hepatic function was studied at intervals in 32 patients with symptoms of portal cirrhosis treated medically for periods less than four months to two and a half years. Pronounced improvement in hepatic function was noted in all patients who continued under medical treatment for longer than four months. The serum bilirubin, the cholesterol cholesterol-ester ratio, the total plasma proteins, the plasma albumin, the urinary urobilinogen and the elimination of hippuric acid roughly paralleled the clinical course. The bromsulfalein excretion test remained abnormal longer than other tests of hepatic function and abnormal values were obtained in 7 of 15 patients so studied. The variations in cephalin cholesterol flocculation, thymol turbidity and alkaline phosphatase did not parallel the clinical course.

Summary Latent portal cirrhosis is more frequent than is realized. In the 50 cases studied, liver biopsy was the most valuable single diagnostic procedure. The disease was encountered twice as frequently in males as in females. Hepatomegaly and splenomegaly were the most frequent physical findings. Esophageal bleeding was the first manifestation of the disease in 8 per cent. Esophageal varices were found by roentgen examination in 13 of 32 patients. Five illustrative cases with latent cirrhosis are reported.

Summary Biopsy specimens were obtained from the livers of 32 patients with portal cirrhosis. The patients were classified in three groups according to whether they were: I-symptom free; II-moderately ill; and III-severely ill, deepjaundiced cases. The specimens were studied histologically in order to determine whether or not the morphologic changes correlated in any way with the clinical status. Repeated biopsy specimens were obtained in 7 cases during the course of medical management.

Bartonella bacilliformis anemia (Oroya fever) is a febrile hemolytic anemia with distinguishing clinical and hematologic characteristics. It occurs as an infrequent clinical form during the invasive stage. The onset is variable with or without chills, followed by a moderate temperature which does not parallel the intensity of the anemia. Hemorrhages, petechial spots, epistaxis may occur and are due to thrombocytopenia. Clouding of the sensorium and delirium are rather uncommon. There is a generalized lymphadenopathy but no splenomegaly. The anemia is macrocytic and frequently hypochromic with signs of intense blood formation: young granulocytes, polychromatophilia, reticulocytosis and nucleated red cells. The reticulocytosis may increase to 50 per cent. The pathognomonic sign of the disease is the presence of bartonella bacilliformis on the erythrocytes. The leukocyte count varies; slight leukocytosis is not uncommon but marked leukocytosis is extremely rare in cases without intercurrent infections. There is a shift of the polymorphonuclear series to the left, characterized by the presence of myeloblasts, myelocytes and metamyelocytes. The anemia is normoblastic and not megaloblastic. It is hemolytic and the destruction of erythrocytes is dependent on the presence of bartonella bacilliformis on the erythrocytes. There is no spherocytosis and the fragility of the erythrocytes is normal. Histologically there is evidence of erythrocyte phagocytosis in the cells of the reticulo-endothelial system; the Kupffer cells, the littoral cells of the spleen and the lymph nodes. The disappearance of the bartonellae from the erythrocytes occurs in a very few days and is called "critical stage" of the anemia. The hematologic changes of this transition are as follows: a change in the shape of the bartonellae from the "bacilliform" to "coccoid" form before complete clearance will take place, an increase in the erythrocyte count, reduction in the indirect hyperbilirubinemia to normal, increase in the number of reticulocytes, reversion to normocytosis, lymphocytosis, reappearance of monocytes and eosinophiles, a "shift to the right" of the polymorphonuclear series. Corresponding with the clearance of bartonella from the erythrocytes, the symptoms dependent on the anemia as well as the fever disappear. Clinical improvement, however, may not parallel the clearance of bartonellae because of intercurrent infections or an atypical course of the bartonellosis itself. Bartonella bacilliformis anemia has a very severe prognosis, due largely to the occurrence of intercurrent infection by enteric organisms. The treatment today is largely symptomatic as there is no specific agent against the bartonellae bacilliformis infection. It is suggested that the prognosis may be improved by the use of adequate blood transfusions and the prophylactic use of antibiotics to control intercurrent infection. At present there is no specific agent against bartonella bacilliformis anemia.

Summary A case of atypical non-alcoholic cirrhosis with diffuse angioma-like dilatation of the sinusoids is described. This apparently is a very rare lesion in man.

Summary and Conclusions Intercurrent infections occurred in nearly half of all hospitalized cases of Carrion's disease studied, and were responsible for the death in two-thirds of the fatal cases. The different intercurrent infections had varied prognosis according to the stage of the disease in which they developed. In cases with Bartonella bacilliformis anemia, intercurrent infections had a very severe prognosis due in most part to the decreased defenses of the host. Septicemias produced by enteric organisms proved to be fatal in almost every instance and accounted for half of the fatalities. The clinical picture in these infected cases consisted in a rise in temperature, diarrhea, splenomegaly, leukocytosis with marked shift to the left in the polymorphonuclear series, followed shortly by death. Amebic colitis greatly resembled the picture produced by salmonellosis and was fatal in three cases observed. Malaria was the most frequent intercurrent infection occurring in approximately one-fourth of the cases. The immunological course of Carrion's disease is not significantly affected by intercurrent malaria infection, as no mortality was recorded in 28 cases. The clinical picture is most cases was very atypical for both diseases, the fever was usually irregular and without the characteristic periodicity of malaria, there was profuse sweating, enlargement of the spleen, anemia and a significant monocytosis. Intercurrent malaria was followed by prompt regression and thrombosis of the verrugae. The host defenses against intercurrent infections did not appear to be decreased during the preeruptive or eruptive stages of Carrion's disease.

Summary In order to determine the meaning and pathogenesis of jaundice in portal cirrhosis, 28 consecutive cases with marked jaundice were studied by simultaneous clinical and histological observation and by conventional biochemical determinations. A previous history of alcoholism was found in 23 of the 28, and an insidious onset of jaundice in 21 of 28. The presence of one or several of the following findings was of considerable importance in establishing the diagnosis of chronic hepatitis: collateral circulation of the abdomen, spider nevi, telangiectasis, hard or nodular liver, and varicose veins of the esophagus. Punch liver biopsy was the most important single diagnostic procedure used, since it served to demonstrate not only liver fibrosis but also changes of the liver parenchyma. Jaundice in patients with cirrhosis represents active parenchymatous liver disease and as such cannot be regarded as a manifestation of "compensated cirrhosis." Pathologically there were active changes of the liver parenchyma; which varied considerably in type and severity. There was no relation between jaundice and the degree or type of fibrosis. Jaundice appeared as a slight, transitory, almost unnoticed episode in the course of chronic hepatitis, or most commonly it was accompanied by other symptoms and findings of liver failure such as edema, ascites, and encephalopathy. Jaundice is considered a very serious sign; its presence contraindicates abdominal surgery. The importance of adequate medical management of portal cirrhosis with jaundice is emphasized, since even patients with severe liver failure can recover clinically. Recovery is accompanied by disappearance of degenerative features, regeneration of the liver parenchyma, and marked improvement of parenchymal function.

Three cases of pyoderma gangrenosum complicating chronic non-specific ulcerative colitis are described in detail. No pathognomonic flora was found and some of the purulent lesions were sterile. Large quantities of sulfonamides and penicillin were of no value either prophylactically or therapeutically. Improvement in Case I followed improvement of the general condition of the patient and persistent local therapy with ultraviolet light and silver nitrate solutions. Complete recovery in Case II was achieved after resection of the infected colon and restoration of a normal state of nutrition. The third patient recovered after use of ultraviolet light therapy, local application of tincture of gentian violet and control of the chronic non-specific ulcerative colitis.

Summary The incidence of symptoms in individuals without roentgenologic evidence of disease and with a gastroscopically normal mucosa does not differ significantly from that observed in patients with "atrophic gastritis" (atrophy), "chronic superficial gastritis" (erythema, edema, exudate), and "hypertrophic gastritis" (cobblestone-appearing mucosa). It is entirely possible, however, that in individual cases the gastrointestinal symptoms may be attributable to erosive and inflammatory processes in the mucosa.

TABLE OF CONTENTS Peptic Ulcer (continued) Surgical Treatment and Results Postgastrectomy Syndrome Postgastrectomy Gastritis Ligation of Vessels Vagotomy—Anatomic and Physiologic Observations Gastric Mucosa After Vagotomy Vagotomy—Favorable Results Vagotomy and Other Surgical Procedures Vagotomy—Restricted Application Postvagotomy Management Recurrence After Vagotomy Vagotomy and Splanchnicectomy Follow-up Studies of Peptic Ulcer and Recurrence Electrolyte Disturbances Massive Hemorrhage General Results Use of Thrombin Surgical Treatment Jejunal Ulcer and Gastrojejunocolic Fistula Perforation Surgical Treatment and Results Nonoperative Treatment Duodenum Motility Bacteriologic Examination Diverticula Tumors Small Intestine Motility—Antispasmodics Absorption Roentgen Observations Meckel's Diverticulum Regional Enteritis Tuberculous Enteritis Acute Pseudomembranous Enteritis Necrotizing Jejunitis Intestinal Lipodystrophy (Whipple's Disease) Steatorrhea and Sprue Absorption of Fat Intussusception Intestinal Obstruction Massive Resection Vascular Lesions Mesenteric Occlusion Malignant Tumors Parasitic and Diarrheal Diseases Epidemic Gastroenteritis Salmonella Infections Bacillary Dysentery Typhoid Parasites Amebiasis Schistosomiasis Lymphogranuloma Venereum Actinomycosis Appendix Acute Appendicitis Tumors Appendices Epiploicae Colon Proctoscopic Examination Megacolon Volvulus Diverticulosis and

Excerpt INTRODUCTION In 1910 Schwartz1enunciated the dictum "no acid—no ulcer" the validity of which has been challenged repeatedly throughout the years. The purpose of this paper is to present a f...

Excerpt The pathogenesis, as well as the treatment, of edema and ascites in portal cirrhosis has been a subject of utmost interest and continuous investigation. Attention has been directed to the r...

The literature pertaining to nonspecific ulcerative colitis continues to emphasize the widely varying concepts of its pathogenesis and treatment.1Although considerable attention has been directed in the past decade to the effects of antibiotics2and to the results of surgical therapy,3observations on the natural history of this disease have been comparatively infrequent.4It seemed of interest, therefore, to review the clinical features and course of nonspecific ulcerative colitis in an illustrative series of 100 patients. The cases were chosen from a group of approximately 250 by the following criteria: completeness of data, length of the period of observation and accurate information as to their present status. There were 14 deaths. Sixty-five of the 86 surviving patients have been reexamined since Jan. 1, 1947; the remainder were restudied in 1946. Because of the method of selection of material to be used in this report, the number of patients

TABLE OF CONTENTS Introduction Esophagus Motility Esophageal Pain Atresia Esophagitis Ulcer Mediastinitis Scleroderma Varices Cardiospasm Carcinoma Stomach Anorexia Nervosa Pernicious Vomiting of Pregnancy Diaphragmatic Hernia Gastric Motility Gastric Secretion Gastroscopy Gastritis Hypertrophic Pyloric Stenosis Foreign Bodies Syphilis Actinomycosis Fibrosis Surgery for Functional Disturbances Peptic Ulcer Historical Incidence Etiology Trauma Roentgenology Treatment Alkalosis Surgical Treatment Massive Hemorrhage Jejunal Ulcer Acute Perforation Ulcer in Childhood Ulcer and Military Service Gastric Cancer Incidence Experimental Production Gastritis and Cancer Prognosis and Classification Natural History Diagnosis Surgical Treatment Benign Tumors Lymphosarcoma Hodgkin's Disease Duodenum Diverticula Obstruction Cyst Rupture Cancer Sarcoma Small Intestine Physiology Roentgenology Anomalies Volvulus Intussusception Stenosis and Adhesions Bezoar Rupture Aneurysm Gallstone Ileus Diverticula Treatment of Intestinal Obstruction Sprue and Related Disorders Regional Enteritis Cyst Benign Tumors Carcinoid Tumors Carcinoma Sarcoma Appendix Acute Appendicitis Etiology Diagnosis Treatment Dysentery and Diarrheal Diseases Epidemic Diarrhea of the Newborn Vitamin Deficiency Food Poisoning Bacillary Dysentery Chemotherapy

CARRION'S disease is caused by Bartonella bacilliformis, a polymorphous organism classified as a bacterium in 1927 by Noguchi, 1 transmitted by sandflies of the genus Phlebotomus. The disease is limited geographically to certain areas of the Andean regions in Peru, Colombia and Ecuador. The disease is extremely polymorphic in symptoms. The confusion existing in the literature arose in part from reports prior to the discovery of B. bacilliformis, when intercurrent infections were not recognized and many symptoms were erroneously assigned to Carrion's disease. The present report is based on a study made on several hundred cases in Lima, Peru, during the period 1938 to 1943. HISTORY AND NOMENCLATURE Archeologic findings indicate that the disease was known in Peru in the pre-Incaic era. Surprisingly accurate representations of the cutaneous nodules, or verrugas, are found in the Peruvian ceramic pots called huacos , especially in the Chimu civilization. 2 The first medical publication

TABLE OF CONTENTS Introduction Books Esophagus General Esophagogastroscope Congenital Atresia Spontaneous Rupture Perforation Foreign Bodies Stricture Diverticula Cardiospasm Peptic Ulcer Cardioesophageal Relaxation Scleroderma Carcinoma Leiomyomas Stomach Gastric Secretion Gastric Motility and Absorption Gastric Cytology Effect of Drugs, Nausea and Emotions Uropepsin Diaphragmatic Hernia Volvulus Diverticula Gastroscopy Experimental Gastritis Symptoms in Patients with Gastritis Large Gastric Rugae Hypertrophic Gastritis Atrophic Gastritis Antral Gastritis Congenital Pyloric Stenosis Pylorospasm Foreign Bodies Gastroileostomy Gastrocolic Fistula Ectopic Smooth Muscle Tuberculosis Gastric Arteriosclerosis Hereditary Hemorrhagic Telangiectasia Polyps and Miscellaneous Tumors Gastric Cancer Survey of Problem Experimental Observations Pernicious Anemia and Gastric Cancer Gastric Secretion Cytologic Elements of Gastric Fluid Metabolic Disturbances Diagnosis Gastroscopy and Gastric Cancer Coexistent Ulcer and Cancer "Carcinomatous Transformation" Unusual Clinical Features Surgical Treatment and Results Peptic Ulcer Experimental Observations Radiation Treatment of Experimental Ulcer Mechanism of Ulcer Pain General Observations Incidence Psychosomatic Relationships Allergy