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Hemorrhagic duodenitis: A significant cause of gastrointestinal bleeding
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Hemorrhagic duodenitis: A significant cause of gastrointestinal bleeding Eugene A. Gelzayd, M.D. Southfield, Michigan
David W. Gelfand, M.D. Detroit, Michigan
Hemorrhagic duodenitis, confirmed by endoscopy and target biopsy, accounted for 8% of acute upper gastrointestinal bleeders treated by these authors. The duodenoscopic and histologic features are described and should lead to more frequent recognition of this postulated entity. Hemorrhagic duodenitis, as a cause of significant acute upper gastrointestinal bleeding, was rarely recognized in the era before duodenoscopy came into routine use. Hemorrhagic duodenitis has been previously described accompanying extensive burns,1 injury to the central nervous system,> tumors of the brain,' major operative procedures,' and myocardial infarction. s The diagnosis usually was made at time of surgery or autopsy. During the course of our continuing study of nonspecific forms of duodenitis,6 we have encountered 8 patients with significant hemorrhage from the duodenum, unassociated with peptic ulcer disease. These patients form the basis of th is report. MATERIALS AND METHODS Fiberduodenoscopic examinations were performed on 8 patients with acute upper gastrointestinal hemorrhage early in the course of their illness. There were 1 black and 7 whites; 7 men and 1 woman. The mean age was 45 years with a range from 28 to 76 years. Detailed histories of previous ulcer disease, parasitic infestation, alcohol and aspirin use, or other gastroduodenal irritants, were obtained. A standard upper gastrointestinal series was performed on 7 of 8 patients. Maximum histalog gastric
analysis, quantitative serum immunoglobulins, and duodenal aspiration of secretions for giardia and other parasites were performed in 5 patients. The Olympus GIF fiberscope was used to examine all patients. Preparation for duodenoscopy consisted of diazepam and atropine. Care was used to avoid traumatizing the duodenal bulb by repeated passage of the instrument through the pylorus. After photography of the duodenum, multiple direct vision mucosal biopsies were taken. RESULTS The duodenoscopic findings in these 8 patients included varying degrees of hyperemia, friability and superficial erosions with active bleeding mainly in the bulb region (Figure 1). Mild hypertrophic nodularity of the bulb and proximal duodenum also was present in 3 patients. No duodenal ulcer or scar was present in any patient. The stomach was normal in all cases. Mild erosive esophagitis without visible bleeding was present in 1 alcohol ic patient. Two other patients with acute and chronic alcoholic liver disease had intact esophageal varices. Six of the 8 patients underwent target mucosal biopsies of the duodenal bulb and proximal duodenum. Histologic evidence of duodenitis was found in each of the 6, and
Figure 1. Hemorrhagic duodenitis: a, massive bleeding during acute myocardial infarction; b, with bleeding erosions after aspirin ingestion; c, following excessive alcohol imbibition. From the Gastroenterology Section, Providence Hospital, Southfield, Michigan, and the Department of Radiology, Detroit General Hospital, Detroit, Michigan. Reprint requests: Eugene A. Gelzayd, M.D., Providence Hospital, 16001 W. Nine Mile Road, Southfield, Michigan 48075. VOLUME 20, NO.2, 1973
60
included superficial ulcerations of the epithelial lining, mild degrees of villous flattening, crypt dilatation, and dense acute and chronic inflammatory cell infiltration of the lamina propria, extending into the Brunner's gland area in 2 patients. Edema, dilated and engorged capillaries, and intramural hemorrhage were also noted. In each of these 6 patients, 2 pathologists independently agreed that significant inflammatory changes were present. Two patients examined in the intensive care unit were not biopsied. Anemia was present in 7 of 8 patients; 4 required multiple blood transfusions. Hematemesis was present in 4 patients and melena in all 8. Dyspeptic epigastric distress in 5 of 8 patients preceded the onset of the bleed by a variable period of time. Two patients were asymptomatic, and a third had onset of massive bleeding during an acute myocardial infarction. A history of significant alcohol intake was present in 4 patients. Aspirin usage prior to bleeding was recorded in 2 patients, myocardial infarction in 1, and severe emotional stress in another. Radiologic findings in 6 of 7 patients studied included spasm and irritabil ity of the bulb and coarse folds in the proximal duodenum. Maximum histalog gastric analysis, quantitative serum immunoglobulins, and direct examination of duodenal secretions for giardia and other parasites were normal in 5 patients. Conservative medical treatment resulted in cessation of bleeding in 7 of 8 patients. One actively bleeding patient expired from his myocardial infarction. One patient with chronic alcoholic liver disease later bled from esophageal varices and eventually required a portacaval shunt. No other patient has subsequently bled over a 2 year follow-up period. Follow-up duodenoscopy and biopsy was performed in 5 patients, 9 to 18 months after the initial bleeding episode. Three of the 5 demonstrated mild patchy hyperemia and friability, 1 demonstrated mild hypertrophic nodularity of the bulb mucosa, and 1 had a normal appearing duodenum. In all 5 patients, histologic inflammatory changes of duodenitis were still present at time of follow-up examination. DISCUSSION Hemorrhagic duodenitis may cause severe upper gastrointestinal bleeding and should be considered in the differential diagnosis of any such patient. Hemorrhagic duodenitis should be particularly suspected in a patient whose upper gastrointestinal x-ray examination fails to show peptic ulcer, esophageal varices, or other obvious cause for the bleeding. A history of alcohol or aspirin intake or severe
emotional or physiological stress may indicate predisposing factors. The 8 patients in this series account for about 8% of our experience with severe upper gastrointestinal bleeding disorders diagnosed in the past 2 years. The pathogenesis of hemorrhagic duodenitis is not firmly established. Our experience,6 and that of Belber,' appears to indicate that alcohol intake may be an important predisposing factor. This observation appears to conflict with that of Pirola et al 8 who found histologically and histochemically normal duodenal mucosa in 6 chronic alcoholics examined after a drinking spree. However, their biopsies were obtained by capsule from the second part of the duodenum. The lack of direct endoscopic control of the biopsy location and the fact that biopsies were taken from the second part of the duodenum, beyond the usual site where hemorrhagic duodenitis occurs, may explain this difference. We also note the previously established relationships of hemorrhagic duodenitis to certain forms of physiologic stress, such as extensive burns,' injury to the central nervous system,> tumors of the brain,' major operative procedures,- and myocardial infarction. s Hemorrhagic duodenitis does not appear to be related to duodenal ulcer in this study. No duodenal ulcer was demonstrated by endoscopy or x-ray in any of the 8 patients. It is possible but unlikely that a small duodenal ulcer might have been invisible to the end-viewing instrument employed in these cases. Hemorrhagic duodenitis also did not appear to be related to esophageal or gastric disease in this group of patients. The endoscopic appearance of the gastric mucosa in 7 of 8 patients was normal. Gastric mucosal biopsies taken in 6 patients were all normal. None of the 5 patients studied demonstrated gastric acid hypersecretion following maximal histalog stimulation. One of the 8 patients had esophagitis at the time of duodenoscopic examination. It would therefore appear that hemorrhagic duodenitis may exist as an entity separate from the known inflammatory diseases of the esophagus and stomach. Conservative medical treatment consisted of nasogastric intubation and suction, correction of anemia, diazepam, antacids and milk, and reassurance. This was sufficient to control the acute bleeding episode in 7 of 8 patients. Conceivably, surgery may be advisable in some cases for uncontrollable hemorrhage. Endoscopic follow-up examinations are recommended in duodenitis patients, much as in ulcer patients who are undergoing a program of therapy.··7
REFERENCES 1. CURLING TB: On acute ulceration of the duodenum in cases of burns. Med Chir Tr London 25:260, 1842 2. DAVIS RA, WETZEL N, DAVIS L: Acute upper alimentary tract ulceration and hemorrhage following neurosurgical operations, Surg Gyn Obst 100:51, 1955 3. CUSHING H: Peptic ulcers and the interbrain.SurgGyn Obst 55:1,1932 4. McDONNELL WV, MCCLOSKEY JF: Acute peptic ulcers as a complication of surgery. Ann Surg 137:67, 1953
5. KATZ AM: Hemorrhagic duodenitis in myocardial infarction. An Int Med 51:212,1959 6. GELZAYD EA, GELFAND OW, RINALDO JA Jr.: Nonspecific duodenitis: a distinct clinical entity: Gastrointestinal Endoscopy 19:131, 1973 7. BELBER )p: Duodenitis: an endoscopist's ruminations. Gastrointestinal Endoscopy 19:57, 1972 8. PIROLA RC. BOLIN DCH, DAVIS AE: Does alcohol cause duodenitis? Arner J Dig Dis 14:239, 1969
GASTROINTESTINAL ENDOSCOPY
Hemorrhagic duodenitis: A significant cause of gastrointestinal bleeding Eugene A. Gelzayd, M.D. Southfield, Michigan
David W. Gelfand, M.D. Detroit, Michigan
Hemorrhagic duodenitis, confirmed by endoscopy and target biopsy, accounted for 8% of acute upper gastrointestinal bleeders treated by these authors. The duodenoscopic and histologic features are described and should lead to more frequent recognition of this postulated entity. Hemorrhagic duodenitis, as a cause of significant acute upper gastrointestinal bleeding, was rarely recognized in the era before duodenoscopy came into routine use. Hemorrhagic duodenitis has been previously described accompanying extensive burns,1 injury to the central nervous system,> tumors of the brain,' major operative procedures,' and myocardial infarction. s The diagnosis usually was made at time of surgery or autopsy. During the course of our continuing study of nonspecific forms of duodenitis,6 we have encountered 8 patients with significant hemorrhage from the duodenum, unassociated with peptic ulcer disease. These patients form the basis of th is report. MATERIALS AND METHODS Fiberduodenoscopic examinations were performed on 8 patients with acute upper gastrointestinal hemorrhage early in the course of their illness. There were 1 black and 7 whites; 7 men and 1 woman. The mean age was 45 years with a range from 28 to 76 years. Detailed histories of previous ulcer disease, parasitic infestation, alcohol and aspirin use, or other gastroduodenal irritants, were obtained. A standard upper gastrointestinal series was performed on 7 of 8 patients. Maximum histalog gastric
analysis, quantitative serum immunoglobulins, and duodenal aspiration of secretions for giardia and other parasites were performed in 5 patients. The Olympus GIF fiberscope was used to examine all patients. Preparation for duodenoscopy consisted of diazepam and atropine. Care was used to avoid traumatizing the duodenal bulb by repeated passage of the instrument through the pylorus. After photography of the duodenum, multiple direct vision mucosal biopsies were taken. RESULTS The duodenoscopic findings in these 8 patients included varying degrees of hyperemia, friability and superficial erosions with active bleeding mainly in the bulb region (Figure 1). Mild hypertrophic nodularity of the bulb and proximal duodenum also was present in 3 patients. No duodenal ulcer or scar was present in any patient. The stomach was normal in all cases. Mild erosive esophagitis without visible bleeding was present in 1 alcohol ic patient. Two other patients with acute and chronic alcoholic liver disease had intact esophageal varices. Six of the 8 patients underwent target mucosal biopsies of the duodenal bulb and proximal duodenum. Histologic evidence of duodenitis was found in each of the 6, and
Figure 1. Hemorrhagic duodenitis: a, massive bleeding during acute myocardial infarction; b, with bleeding erosions after aspirin ingestion; c, following excessive alcohol imbibition. From the Gastroenterology Section, Providence Hospital, Southfield, Michigan, and the Department of Radiology, Detroit General Hospital, Detroit, Michigan. Reprint requests: Eugene A. Gelzayd, M.D., Providence Hospital, 16001 W. Nine Mile Road, Southfield, Michigan 48075. VOLUME 20, NO.2, 1973
60
included superficial ulcerations of the epithelial lining, mild degrees of villous flattening, crypt dilatation, and dense acute and chronic inflammatory cell infiltration of the lamina propria, extending into the Brunner's gland area in 2 patients. Edema, dilated and engorged capillaries, and intramural hemorrhage were also noted. In each of these 6 patients, 2 pathologists independently agreed that significant inflammatory changes were present. Two patients examined in the intensive care unit were not biopsied. Anemia was present in 7 of 8 patients; 4 required multiple blood transfusions. Hematemesis was present in 4 patients and melena in all 8. Dyspeptic epigastric distress in 5 of 8 patients preceded the onset of the bleed by a variable period of time. Two patients were asymptomatic, and a third had onset of massive bleeding during an acute myocardial infarction. A history of significant alcohol intake was present in 4 patients. Aspirin usage prior to bleeding was recorded in 2 patients, myocardial infarction in 1, and severe emotional stress in another. Radiologic findings in 6 of 7 patients studied included spasm and irritabil ity of the bulb and coarse folds in the proximal duodenum. Maximum histalog gastric analysis, quantitative serum immunoglobulins, and direct examination of duodenal secretions for giardia and other parasites were normal in 5 patients. Conservative medical treatment resulted in cessation of bleeding in 7 of 8 patients. One actively bleeding patient expired from his myocardial infarction. One patient with chronic alcoholic liver disease later bled from esophageal varices and eventually required a portacaval shunt. No other patient has subsequently bled over a 2 year follow-up period. Follow-up duodenoscopy and biopsy was performed in 5 patients, 9 to 18 months after the initial bleeding episode. Three of the 5 demonstrated mild patchy hyperemia and friability, 1 demonstrated mild hypertrophic nodularity of the bulb mucosa, and 1 had a normal appearing duodenum. In all 5 patients, histologic inflammatory changes of duodenitis were still present at time of follow-up examination. DISCUSSION Hemorrhagic duodenitis may cause severe upper gastrointestinal bleeding and should be considered in the differential diagnosis of any such patient. Hemorrhagic duodenitis should be particularly suspected in a patient whose upper gastrointestinal x-ray examination fails to show peptic ulcer, esophageal varices, or other obvious cause for the bleeding. A history of alcohol or aspirin intake or severe
emotional or physiological stress may indicate predisposing factors. The 8 patients in this series account for about 8% of our experience with severe upper gastrointestinal bleeding disorders diagnosed in the past 2 years. The pathogenesis of hemorrhagic duodenitis is not firmly established. Our experience,6 and that of Belber,' appears to indicate that alcohol intake may be an important predisposing factor. This observation appears to conflict with that of Pirola et al 8 who found histologically and histochemically normal duodenal mucosa in 6 chronic alcoholics examined after a drinking spree. However, their biopsies were obtained by capsule from the second part of the duodenum. The lack of direct endoscopic control of the biopsy location and the fact that biopsies were taken from the second part of the duodenum, beyond the usual site where hemorrhagic duodenitis occurs, may explain this difference. We also note the previously established relationships of hemorrhagic duodenitis to certain forms of physiologic stress, such as extensive burns,' injury to the central nervous system,> tumors of the brain,' major operative procedures,- and myocardial infarction. s Hemorrhagic duodenitis does not appear to be related to duodenal ulcer in this study. No duodenal ulcer was demonstrated by endoscopy or x-ray in any of the 8 patients. It is possible but unlikely that a small duodenal ulcer might have been invisible to the end-viewing instrument employed in these cases. Hemorrhagic duodenitis also did not appear to be related to esophageal or gastric disease in this group of patients. The endoscopic appearance of the gastric mucosa in 7 of 8 patients was normal. Gastric mucosal biopsies taken in 6 patients were all normal. None of the 5 patients studied demonstrated gastric acid hypersecretion following maximal histalog stimulation. One of the 8 patients had esophagitis at the time of duodenoscopic examination. It would therefore appear that hemorrhagic duodenitis may exist as an entity separate from the known inflammatory diseases of the esophagus and stomach. Conservative medical treatment consisted of nasogastric intubation and suction, correction of anemia, diazepam, antacids and milk, and reassurance. This was sufficient to control the acute bleeding episode in 7 of 8 patients. Conceivably, surgery may be advisable in some cases for uncontrollable hemorrhage. Endoscopic follow-up examinations are recommended in duodenitis patients, much as in ulcer patients who are undergoing a program of therapy.··7
REFERENCES 1. CURLING TB: On acute ulceration of the duodenum in cases of burns. Med Chir Tr London 25:260, 1842 2. DAVIS RA, WETZEL N, DAVIS L: Acute upper alimentary tract ulceration and hemorrhage following neurosurgical operations, Surg Gyn Obst 100:51, 1955 3. CUSHING H: Peptic ulcers and the interbrain.SurgGyn Obst 55:1,1932 4. McDONNELL WV, MCCLOSKEY JF: Acute peptic ulcers as a complication of surgery. Ann Surg 137:67, 1953
5. KATZ AM: Hemorrhagic duodenitis in myocardial infarction. An Int Med 51:212,1959 6. GELZAYD EA, GELFAND OW, RINALDO JA Jr.: Nonspecific duodenitis: a distinct clinical entity: Gastrointestinal Endoscopy 19:131, 1973 7. BELBER )p: Duodenitis: an endoscopist's ruminations. Gastrointestinal Endoscopy 19:57, 1972 8. PIROLA RC. BOLIN DCH, DAVIS AE: Does alcohol cause duodenitis? Arner J Dig Dis 14:239, 1969
GASTROINTESTINAL ENDOSCOPY