A particular case of acute necrotizing pancreatitis

Letters to the Editor Helicobacter pylori and complicated ulcer disease To the Editors: In the excellent review article on Helicobacter pylori and the gastroduodenal mucosa, Kokoska and Kauffman1 state that it is unknown if the rate of H pylori infection is similar in those with and without complicated ulcer disease. They further speculate that standard surgical acidreducing procedures might be replaced by medical therapy directed at H pylori. We would offer a different viewpoint. Work at our institution and others had demonstrated an H pylori infection rate much lower in those with complicated ulcers versus those reported in other cohorts.1-6 Obstruction and bleeding requiring surgical intervention had H pylori infection rates no higher than 33% to 70%. While H pylori and nonsteroidal anti-inflammatory use may account for the majority of gastroduodenal ulcers, the underlying cause of complicated ulcers requiring surgical intervention may include other factors such as acid hypersecretion. The implications for the general surgeon are important. Deviation from traditional acid-reducing procedures (or no procedure at all) in the H pylori negative cohort could lead to recurrent obstruction or bleeding. Hopefully, further analysis from other institutions will add to our knowledge in this area. For the present, however, we believe traditional surgical principles directed at an acid-reducing procedure should continue to be used in those requiring operation for complicated ulcer disease. Stephen W. Behrman, MD Department of Surgery The University of Tennessee 956 Court Ave Memphis, TN 38163 References 1. Kokoska ER, Kauffman, GL. H. pylori and the gastroduodenal mucosa. Surgery 2001;130:13-6. 2. Gibson JB, Behrman SW, Fabian TC, et al. Gastric outlet obstruction resulting from peptic ulcer disease requiring surgical intervention is infrequently associated with H. pylori. J Am Coll Surg 2000;191:32-7. 3. Perng C, Lin H, Lu W, et al. Characteristics of patients with benign gastric outlet obstruction requiring surgery after endoscopic balloon dilation. Am J Gastroenterol 1996;91: 987-90. 4. Lam Y. Endoscopic balloon dilation and H. pylori eradication in the treatment of gastric outlet obstruction. Gastrointest Endosc 1999;46:379-80. 5. Callicutt CS, Behrman SW. Incidence of H. pylori in operatively managed acute nonvariceal upper gastrointestinal bleeding. J Gastrointest Surg 2001;5:614-9. 6. Fisher D, Hussbaum M, Pritts T, et al. Use of omeprazole in the management of giant duodenal ulcers: results of a prospective study. Surgery 1999;126:643-9.

7. Tokunaga Y, Hanta K, Ryo J, et al. Density of H. pylori infection in patients with peptic ulcer perforation. J Am Coll Surg 1998;186:659-63. 11/59/123477 doi:10.1067/msy.2002.123477

Reply To the Editors: We appreciate the comments from Stephen W. Behrman, MD, and the opportunity to respond. The basic premise stated by Dr Behrman is that complicated peptic ulcer disease may not always result from Helicobacter pylori infection. We definitely concur with this concept. We believe there are 3 goals of surgical treatment for complicated peptic ulcer disease. First, the acute problem (perforation, bleeding, etc) should be addressed. Second, the presence of cancer should be ruled out if the ulcer is of gastric origin. Finally, ulcer recurrence should be minimized. If the cause of the ulcer is believed to be related to H pylori infection, as evidenced by endoscopic findings or a positive rapid urease test, subsequent management should involve antibiotic therapy targeting this organism and further surgery directed toward acid reduction may not be necessary. This was 1 point of our review article. If, however, the ulcers do not appear to be related to H pylori infection, surgical efforts to limit acid secretion are likely warranted. Evan R. Kokoska, MD JW Riley Hospital for Children Suite 2500; 702 Barnhill Drive Indianapolis, IN 46202 Gordon L. Kauffman, Jr, MD Penn State University Hershey, Pa 11/59/123478 doi:10.1067/msy.2002.123478

A particular case of acute necrotizing pancreatitis To the Editors: It is generally accepted to treat acute sterile necrotizing pancreatitis conservatively.1 In the following case, we were confronted with an exceptional course of acute necrotizing pancreatitis in which laparotomy was inevitable. A 71-year-old man was referred with history, physical examination, and laboratory results indicating acute pancreatitis due to biliary stones or excessive alcohol intake. An abdominal ultrasound and magnetic resonance cholangiopancreatography, however, showed no gallstones or dilated bile ducts. The patient was admitted and treated with restricted oral intake, intravenous fluid SURGERY 589

590 Letters to the Editors

Fig 1. Computed tomography scan showing a retroperitoneal mass filled with air, signs of pancreatic necrosis, and free air intraperitoneally. replacement, and antibiotics. A Ranson score of 4 classified the pancreatitis as severe. The following day, the patient had increasing back pain. A computed tomography scan showed a retroperitoneal mass filled with air and free air under the right hemidiaphragm, which suggested a perforated hollow viscus (Figure). The pancreas showed signs of necrotizing pancreatits. At laparotomy, air escaped at the opening of the peritoneal sac. Profound necrosis was found in the caput and corpus of the pancreas. A thorough abdominal inspection and administration of methylene blue via the gastric tube failed to demonstrate a gastrointestinal perforation. Débridement of necrotic pancreatic tissue and cholecystectomy of a macroscopically non-inflamed, intact gallbladder were performed. Postoperative treatment was instituted with intravenous imipenem in the intensive care unit. Intraoperative cultures of pancreas necrosis showed a Clostridium perfringens infection, which is susceptible to imipenem. Microscopic evaluation showed chronic inflammation of the gallbladder, and cultures revealed Clostridium perfringens. Recurrent pancreatic abscesses necessitated percutaneous computed tomography–guided drainage. After returning to the surgical ward, the patient gradually recovered in the next 3 months, until he died suddenly of cardiac arrest. At autopsy, the pancreas appeared completely destroyed, and several abscesses were found in the abdominal cavity and pancreatic region. In this case, 2 particular findings are reported: First, a patient with an acute necrotizing pancreatitis infected with Clostridium perfringens; and second, a patient with this gas-producing bacteria in the retroperitoneal compartment, which exhibited free air intraperitoneally.

Surgery May 2002 Only 5 case reports in the past 2 decades report on Clostridium perfringens–infected pancreatic necrosis with characteristic signs of retroperitoneal gas.2-6 This is the first case reporting free intraperitoneal air. Pancreatic necrosis is generally infected by common intestinal organisms. Foitzik et al6 describe migration of Clostridium perfringens from the bile ducts to the pancreas. The gallbladder in the present case was infected with Clostridium perfringens, which most likely migrated to the necrotic pancreas. After diffusing to the lesser sac, the retroperitoneal gas entered the abdominal cavity via the foramen of Winslow, allowing free air under the diaphragm. The management of acute pancreatitis is initially conservative depending on its severity as judged by the Ranson score. If suspected, infected pancreatic necrosis should be verified by percutaneous fine needle aspiration. In a case of infection, débridement should be performed. If there are no signs of infection, further conservative management using antibiotics is safe.1 In the present case, conservative treatment using imipenem would have been instituted if no intraperitoneal air was found. The presence of free intraperitoneal air, however, justified laparotomy. E. M. Noorda, MDa A. P. J. Houdijk, MD, PhDa P. Snel, MD, PhDb B. J. Dwars, MD, PhDa aDepartment of Surgery bDepartment of Gastroenterology Slotervaartziekenhuis Louwesweg 6, 1066 ED Amsterdam, The Netherlands References 1. Buchler MW, Gloor B, Müller CA, Friess H, Seiler CA, Uhl W. Acute necrotizing pancreatitis: treatment strategy according to the status of infection. Ann Surg 2000;232:619-26. 2. Levy P, Boudet MJ, Perniceni T, Mal F, Leguillou JL, Lamer C, et al. Spontaneous gas gangrene of the pancreas caused by Clostridium perfringens. Gastroenterol Clin Biol 1999;23: 1248-50. 3. Sadeghi-Nejad H, O’Donnell KF, Banks PA. Spontaneous gas gangrene of the pancreas. J Clin Gastroenterol 1994; 18:136-8. 4. Faintuch J, Menicino MT, Speranzini MB, Pinotti HW, Smolentsov H. Clinical regression of infected pancreatic necrosis. Case report. Int J Pancreatol 1991;8:379-86. 5. Raahave D, Hron T. Gas gangrene of the omental bursa following acute pancreatitis. Scand J Infect Dis 1984;16:207-9. 6. Foitzik T, Quentmeier A, Klar E, Buhr HJ, Herfath C. Pneumoperitoneum in a patient with acute biliary pancreatitis. Eur J Surg 1996;162:507-9. 11/59/123012 doi:10.1067/msy.2002.123012