valuable information regarding the functions of the stomach may be obtained. 2. Only a fraction of the fasting contents can be obtained by means of the ordinary stomach tube, in fact, the quantity secured in this way may represent but one-quarter to one-half of the entire fasting secretion of the stomach. It is therefore important, when exact information regarding the volume of the residuum is desired, that the Rehfuss tube should be used in preference to the Ewald tube. Ordinarily, however, the volume of the residuum secured by means of the Ewald tube is relatively constant, so that the results obtained in this manner may be assumed to be sufficiently accurate for clinical purposes. 3. The microscopic examination of the fasting contents is by far more important than the estimation of the volume secured. The secretion can usually be as well obtained for this purpose by means of the Ewald tube as with the Rehfuss tube. We desire to acknowledge our thanks to Dr. Julius Friedenwald through whose advice and under whose direction this work was conducted. REFERENCES FOWLER, REHFUSS AND HAWK: Jour (8) WHITE: Jour. Amer. Med. Assoc., October 28, 1922, lxxix, 1409. Assoc. Amer. Physicians, 1922, 37-86. (9) FRIEDENWALD, Gantt and MORRISON: Studies in fractional analyses. Ann. Clin. Med., March, 1924, ii, no. 5, 292. (10) KOPELOFF: Jour. Amer. Med. Assoc., February 18, 1922, lxxviii, 6; 405. Massive Hemorrhage from the Stomach Produced by an Unusual Cause1 BY JULIUS FRIEDENWALD AND PAUL F. WIEST, Baltimore, Maryland M ASSIVE hemorrhages from the stomach may occur from a variety of causes. In general, these may be classified as follows: 1. Gastric and duodenal ulcer. 2. Cancer. 3. Exulceratio simplex (Dieulafoy). 4. Hemorrhagic gastritis. 5. Hepatic affections (cirrhosis, epidemic jaundice, acute yellow atrophy). 6. Splenic disease (anemia, Banti's disease). 7. Constitutional and toxic diseases (leukemia, hemophilia, yellow fever, phosphorus poisoning). The relation of disease of the blood vessels to gastric ulcer and consequently to hemorrhage was pointed out clearly by Virchow (1) in 1853, though even many years before. Cruveilhier (1829-1835) had called attention to this fact. Virchow maintains that ulceration is preceded by localized disease and obstruction of the arteries which finally terminates in hemorrhagic necrosis. Since this publication numerous observations have been recorded directing attention to the importance of localized arterial disease as a factor in the patho 8. Aortic aneurysm with rupture into genesis of gastric and duodenal ulcer. the stomach. 9. Trauma over the stomach. 10. Vicarious menstruation. 11. Localized arterio-sclerosis of the gastric vessels. It is not the object of this paper to review the problems concerned in the etiology of the various forms of gastric hemorrhage but especially to call attention briefly to that variety of bleeding noted last in this classification; that due to localized disease of the gastric vessels. 1 From the Gastro-Enterological Clinic of the Department of Medicine, University of Maryland. Presented at the meeting of the American Gastro-Enterological Association, May 5, 1924. Of these the works of Merkel (2) and Hauser (3) are especially valuable as pointing to the part played by arteriosclerosis in the production of this disease. Riesman (4) in an interesting paper on hemorrhage in the course of Bright's disease states that Fisher reported four cases of hematemesis associated with small white kidneys and that Bonifas reported a case of severe gastric hemorrhage in a nephritic patient of thirty. Riesman concludes that Bright's disease may cause hemorrhage from the nose, uterus, lungs; into the brain, eye, ear and stomach, and also a more or less well-marked hemorrhagic diathesis with bleeding into the skin and mucous membranes. The true cause of the hemorrhagic diathesis is unknown, but it is probably a toxin analogous to the hemorrhagins of snake venom. In the other types of bleeding, arterial diseases and hypertension are the chief factors. In 1913 Ophüls (5), in a most important communication, calls attention to the results of his observations in a study of 1500 autopsies in which he demonstrates the close relation of disturbances of the blood supply in definite limited areas on the mucous membrane to the production of gastric and duodenal ulceration. He also points out, that the most common type of ulcer is the arterio-sclerotic variety occurring in individuals past the thirtieth year of age. A similar conclusion was arrived at by Stockton (6). In 2 cases reported by Simon (7) the X-ray indicated the presence of former duodenal ulceration, but inasmuch as both individuals presented evidences of arterial disease, he concludes that the profuse and recurrent hemorrhages noted in his cases had their origin in an ulceration due to arterio-sclerosis. Aside from the hemorrhages occasioned by ulceration due to arteriosclerosis, Simon notes that the associated hypertension of the arterial vessels plays a most important rôle in the production of this condition. He observed in his cases, that with each attack there was a sudden fall in blood pressure followed quickly by an equally rapid rise to the readings noted previous to the hemorrhage and concludes that the copious discharge of blood serves as a "safety valve" in blood letting relieving the general hypertension. However, while hemorrhages occur not uncommonly due to rupture of arterio-sclerotic vessels in gastric and duodenal ulcers, arterial rupture is possible in a similar condition of the vessels of the stomach without ulceration much like that observed in cerebral apoplexy due to arteriosclerotic changes in the vessels of the brain. Due to an increase in blood pressure the wall of the artery weakened by this disease may rupture causing profuse hemorrhage. In connection with this character of hemorrhage brief histories of the following 2 cases, presenting an almost identical symptomatology are of interest. Case 1. J. S., male, aged seventy-two years, had complained of weakness, dyspnea, swellings of his legs and headaches for several months. He had at no time ex perienced indigestion with the exception of a slight distention and constipation; nor had nausea, vomiting or hematemesis ever been noted. On physical examination the radials were markedly thickened and the temporal arteries were tortuous and full. The blood pressure was 190 systolic and 120 diastolic. The heart was markedly enlarged to the left and a loud systolic bruit at the apex with a slight arrhythmia was noted. The abdomen was soft and no enlargements or tender areas were detected. The liver and spleen were not palpable. The urine was of a specific gravity of 1015 and contained a few hyaline casts but no albumin. The phthalein kidney function was 25 per cent for the first hour and 23 per cent for the second, a total of 48 per cent. A diagnosis of mitral insufficiency, cardiac hypertrophy, myocarditis with cardiac decompensation was made. The patient was placed at rest in bed upon a Karell diet and digitalis therapy with nightly administrations of hypodermic injections of morphia. He improved for a week under this treatment; the edema and dyspnea gradually disappeared and he expressed himself as greatly relieved, though at no time had the blood pressure been reduced. Suddenly ten days following this treatment he was awakened at night with nausea, and vomited over a quart of bright red blood contents and died within a few hours. At a partial autopsy, the stomach was found filled with blood-stained material and clots. The right and left gastric arteries and the right and left gastro-epiploics were much thickened and a large rupture noted in the right gastric artery near the pylorus. No evidence of ulceration whatever could be detected. The liver was not enlarged and with the exception of fatty degenerative changes in the liver cells nothing abnormal was noted. Case 2. A. P., male, aged sixty-four years, had been affected with dyspnea upon exertion, lack of appetite, weakness, loss of flesh, and gaseous distention for a period of about six months. These symptoms though of a mild type at first, had steadily become aggravated, so that the patient was unable to move about any distance with comfort. His nights were especially uncomfortable, the dyspnea and distention becoming markedly increased at this time. The patient had experienced no indigestion previously, and had at no time vomited blood or passed tarry stools. On physical examination he was found to be emaciated and anemic. His radials were compressed with difficulty; blood pressure 210 systolic, 140 diastolic. The heart was enlarged to the left and the heart beats rapid (118 at rest; 128 upon exertion); no murmurs could be elicited. The aortic second sound was accentuated. The abdomen was soft and relaxed and there were no palpable masses. The urine showed a specific gravity of 1012; albumin and hyaline and granular casts were present in abundance. A phenolsulphonephthalein test revealed a percentage of 12 for the first hour and 16 for the second, making a total of 28 per cent. The blood Wassermann was negative. The diagnosis of chronic nephritis with hypertension and cardiac hypertrophy was made. The patient was ordered to rest in bed and placed upon a soft diet and digitalis therapy was instituted; in spite of this régime, signs of improvement were not noted and the dyspnea and abdominal distention became more aggravated, though pain was at no time present. At the end of the second week, two slight gastric hemorrhages occurred on the same day. These were followed by the passage of soft tar-colored stools. The hemorrhages were accounted for at this time upon the basis of a passive congestion of the stomach, though there was no evidence of any enlargement of the liver or of free fluid in the abdomen or edema of the extremities. The systolic blood pressure readings continued over 200 mm. After another week without any improvement, the patient, while at rest during the day, experienced an attack of nausea which was followed by the vomiting of at least 2 quarts of bright red blood, food remnants and clots. His pulse now became thready, his respiration rapid and labored; a clammy perspiration appeared and he died within an hour. At a partial autopsy, the stomach was observed to be filled with blood clots. The blood vessels of the stomach were markedly sclerosed and a rupture in the right gastric artery was detected and was the evident source of the hemorrhage; no ulceration was noted anywhere in the stomach. The liver was found but slightly enlarged and one section showed some areas of cirrhosis. The kidneys were small and cirrhotic and presented the usual picture of a chronic interstitial nephritis. The 2 cases illustrate the fact that great care should be exercised in the diagnosis of gastric and duodenal ulceration from hemorrhage alone, inasmuch as this condition may arise as a result of other affections. It may occasionally occur in elderly individuals from a rupture of an arteriosclerotic vessel in the stomach without ulceration. |