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was fibrosis. 80% of cases showed a slight inflammatory cell infiltrate whilst 60% showed activated lymphoid follicles with large germinal centres. In 28% lymphoid hyperplasia was recorded. Ultrasound has high sensitivity and specificity in the diagnosis of acute appendicitis, but false-positive and falsenegative results still occur and the decision to operate remains a clinical one. So far, there are few reported cases of chronic appendicitis, but the increased use of ultrasound may reveal that chronic or subacute appendicitis is more common than we had supposed.
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REFERENCES 1 Sivet CJ, Newman KD, Boenning DA, et al. Appendicitis: usefulness of ultrasound in diagnosis in a pediatric population. Radiology 1992;185:549-52 2 Siegel MJ. Acute appendicitis in childhood: the role of ultrasound. Radiology 1992;185:341-2 3 Seidmen JD, Andersen DK, Ulrich S, et a]. Recurrent abdominal pain due to chronic appendiceal disease. South MedJ 1991;84:913-16 4 Rioux M. Sonographic detection of the normal and abnormal appendix. AmJ Roentgenol 1991;158:773-8 5 Falk S, Schutze U, Guth H, et a]. Chronic recurrent appendicitis. A clinicopathologic study of 47 cases. EurJ Pediatr Surg 1991;1:277-81
Double pylorus as a cause of gastrointestinal bleeding Dirk Ehrhardt
Matthias Lohr
Stefan Liebe
J R Soc Med 1999;92:253-254
MM The most common causes of upper gastrointestinal tract bleeding are peptic ulcer, haemorrhagic gastritis, oesophageal varices, Mallory-Weiss syndrome, and tumours; haemangiomas and bleeding from the biliary tract contribute a few casesl. For a double pylorus to present in this way is very unusual. CASE HISTORY
A man aged 57 was admitted via the emergency room with haematemesis and severe epigastric pain. He was an alcoholic and a smoker. 9 years previously a gastric ulcer had been diagnosed radiologically (but not endoscopically) and treated with H2-receptor antagonists; thereafter he had been free of abdominal pain until the present episode. There had been no melaena. On examination he was normotensive but anaemic (haemoglobin 7.9 g/dL, haematocrit 37%). Quick test was 76% normal, activated prothrombin time 28.7 s. At endoscopy there was no blood in the stomach but clot was seen adhering to the stomach wall in the prepyloric region. This could not be removed with forceps. Gastric Division of Gastroenterology, Klinik fur Innere Medizin, Universitat Rostock, Germany
Correspondence to: Professor M Lohr, Division of Gastroenterology, Department of Intemal Medicine, University of Rostock, E. Heydemann Str. 6, D-18055 Rostock, Germany E-mail:
[email protected]
Figure 1 Endoscopic appearance of gastric outlet with view of double pylorus
ulcer was diagnosed and he was treated with intravenous omeprazole 40 mg twice daily and intravenous amoxycillin 100 mg three times daily. Within a few days the abdominal pain ceased entirely. At a second endoscopy there were no signs of gastric bleeding, but in the prepyloric antrum the entrance to a fistula was suspected (Figure 1). Double pylorus was confirmed by side-view duodenoscopy, cannulation and contrast radiography (Figure 2). Thenceforth the patient's course was unremarkable, apart from development of gouty arthritis in the left foot which responded to colchicine. He was discharged on day 14 and did not return for follow-up. COMMENT
A duplicated gastric outlet is thought to arise in two ways. A congenital double pylorus is a rare anomaly caused by gastric and duodenal duplication3'4. An acquired double pylorus is a complication of prepyloric or postpyloric ulcer, which perforates the gastric and duodenal walls and gives rise to a fistula. The prevalence in routine endoscopic and radiodiagnostic procedures is estimated at between 0.02 and 0.13%5, with a distinct overrepresentation of males6. The ulcers that give rise to these fistulas commonly show themselves by bleeding, and there is often an underlying disease such as alcoholism, diabetes or chronic renal
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eradication of Helicobacter pylori. (In some cases there had been rupture of the bridging tissue between the original pylorus and the gastroduodenal fistula, and the endoscopist may mistake this appearance for a normal pyloric channel.) Clearly, the treatment of double pylorus should always include eradication of H. pylori.
REFERENCES Figure 2 Contrast radiograph of pyloric channel with catheter in one of the communications between stomach and duodenal bulb (arrow)
failure6 9. Many patients have ulcer disease of long duration. In uncomplicated double pylorus there may be few symptoms or none6'9. When did the fistula develop in our patient? One possibility is that it resulted from the previous ulcer 9 years earlier, with secondary bleeding now. Another is that this was a fresh ulcer, bleeding as it penetrated the duodenum. The first interpretation is supported by the work of Tsung-Hui et al. 10, who in double-pylorus channels found ulcers that healed only after successful
Duodenal diverticulum as a cause of massive gastrointestinal bleeding L S Wong MD FRCS S Hobbs MB ChB N J Dorricott ChM FRBS J R Soc Med 1999;92:254-255
Duodenal diverticula are usually identified as an incidental finding at endoscopy or in barium studies. The complications arise from pressure effects or from inflammation. Department of Surgery, Selly Oak Hospital, Birmingham B29 6JD, UK
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Correspondence to: Mr L S Wong, 21 Furrows Close, Littlethorpe, Leicester LE9 5JR, UK
I Herold G, Diehl V, Erdurann E, et al. Innere Medizin. Cologne: G Herold, 1995:355 2 Stannard M, Curranio G, Splawski J. Congenital double pylorus with accessory pyloric channel communicating with an intraluminal duplication cyst of the duodenum. Pediatr Radiol 1993;23:48-50 3 Yoshimura Y, Yasutake K, Imsamura Y, Oimomi M. Double pylorus accompanied by gastric ulcer resistant to H2-receptor antagonist a case report and review of the literature. Kobe J Med Sci 1988;34: 151-9 4 Polloni A, Marchi S, Bellini M, Costa F, Bonifazi V, Tumino E. Double pylorus: report of two cases and a review of the literature. Ital J Gastroenterol 1991 ;23:360-3 5 Graham M, Lin F, Flowers J. Symptomatic double-channel pylorus: successful treatment with a biliary sphincterotomy. Surg Endosc 1994;8:792-3 6 Yousuf M, Kameyda S, Noda A, Watanabe T. A case of double pylorus accompanied with adrenal adenoma. Am J Gastroenterol 1989;2:173-5 7 Varrela R, Gallego E, Garcia V. Double pyloric canal: presentation of 3 new cases and a review of the literature. Rev Esp Enferm Apar Dig 1989;75: 185-7 8 Welscher G, Schwab G, Glaser K, Fend F, Bodner E, Pointner R. Dieulafoy lesion in a congenital double pylorus. Endoscopy 1994;26: 374-5 9 Hu TH, Tai DI, Changchien CS, Chen TY, Chang WC. Double pylorus: report of a longitudinal follow-up in two refractory cases with underlying disease. Am J Gastroenterol 1995;90:815-18
CASE HISTORY
A woman of 60 with ischaemic heart disease and noninsulin-dependent diabetes mellitus was seen at another hospital with melaena and syncope. She had experienced vague gastrointestinal symptoms for 14 years but had not bled; there was no story of excessive alcohol intake. Coronary artery bypass surgery had been unsuccessful and she was on various cardiac medications including aspirin. On physical examination she was profoundly pallid and had mild upper abdominal tenderness. The abdomen was somewhat distended with active bowel sounds. Haemoglobin was 4.4 g/dL with a mean cell volume of 64.5 fL suggestive of acute on chronic bleeding. After further passage of melaena stools she deteriorated rapidly and became hypotensive. She was transfused with 6 units of blood and transferred to our institution, where she had one episode of haematemesis. On emergency endoscopy with an end-viewing instrument fresh blood was seen coming from
