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Digestive Diseases and Sciences, Vol. 48, No. 8 (August 2003), pp. 1472–1474 (C© 2003)

CASE REPORT

Necrotizing Acute Pancreatitis Inducedby Salmonella typhimurium

ANDREW BLANK, MD,* MAJID MAYBODY, MD, † GINGER ISOM-BATZ, MD,‡MITCHELL ROSLIN MD,‡ and EVAN H. DILLON MD†

KEY WORDS: Salmonella; necrotizing; pancreatitis.

Salmonella is a gram-negative, non-spore-forming,motile, facultatively anaerobic bacillus. It may presentwith gastroenteritis, enteric fever, bacteremia, or as anasymptomatic carrier state. Typhoid fever is most com-monly caused byS. typhiandS. paratyphi. Enteric fever ismore common in developing countries and is rarely seenindigenously in the United States. It is transmitted viafecal–oral contamination of water and food and is char-acterized by prolonged fevers, abdominal pain, diarrhea,intestinal bleeding, rose spots, and splenomegaly. Non-typhusSalmonella(S enteritidisandS typhimuriummostcommonly) account for about 2.3% of gastroenteritis casesin the United States, or 2–4 million cases annually. Theyare most often associated with poultry and eggs and mayalso be seen with meat and dairy products. The spectrumof disease of nontyphusSalmonellaranges from mild tocholeralike. Fever, abdominal cramping, nausea, vomit-ing, or chills may also be present. The disease is seen asa complication of other diseases such as AIDS, cirrhosis,diabetes, malaria, and sickle cell anemia. Unusual man-ifestations include osteomyelitis, aneurysms, meningitis,and appendicitis.Salmonellapancreatitis is a rare entitythat has also been reported. Here we describe a case of aneven rarer association ofS. typhimuriumcausing a necro-tizing pancreatitis.

CASE REPORT

A 64-year-old Russian-speaking female presented to theLenox Hill Hospital emergency room with generalized weak-ness, diarrhea, with nausea and vomiting for four days prior to

Manuscript received February 15, 2003; revised manuscript receivedApril 29, 2003; accepted May 10, 2003.

From the *Section of Gastroenterology,†Department of Radiology,and‡Department of Surgery, Lenox Hill Hospital, and New York Uni-versity School of Medicine, New York, New York, USA.

Address for reprint requests: Andrew Blank, MD, Lenox Hill Hospital,Section of Gastroenterology, 100 East 77th St, 3 Achelis, New York, NewYork 10021, USA.

admission. No blood in stool was noted. She described ecchymo-sis over the umbilical area. The patient denied any hemateme-sis, fevers, jaundice, NSAID use, or recent travel history. Shereported minimal alcohol use. There was no history of ulcer dis-ease, reflux, or consumption of undercooked foods. She was em-pirically placed on amoxicillin clavulanate for three days priorto admission.

Physical findings on admission included a heart rate of 131beats per minute. The blood pressure was 144/54 mm Hg.She was afebrile. The abdomen was not tender. The skin sur-rounding the umbilicus and the right side of the abdomenwas ecchymotic. Serum amylase and lipase were normal. Thewhite blood cell count was 13,900 with 44% bands, hematocrit48.0%, LDH 5049 units/liter, calcium 7.9 mg/dl, and bicarbon-ate 17 meq/liter. Her glucose was 270 mg/dl, albumin 3.1 g/dl,and blood urea nitrogen 30 mg/dl, giving an overall Glasgowscore of 5.

An abdominal x-ray demonstrated a sentinel loop. Computer-ized tomography showed a 7-× 10-cm inflammatory mass con-taining collections of gas in the head and body of the pancreaswith no evidence of extravasated barium (Figure 1). Gallstoneswere not present. An upper Gastrointestinel series confirmed nofistulous tract was present.

The patient was admitted to the surgical intensive care unitand started on broad-spectrum parenteral antibiotics. She wasmade NPO and given parenteral fluids. A nasogastric tube wasplaced. The decision for surgery was made on hospital day 2 dueto continued acidosis and fever to 102◦F. Exploratory laparotomywas performed with pancreatectomy, pancreatic debridement ofnecrotic tissue, and insertion of two sump drains. Gross necrosisand hemorrhagic infarct was found in virtually the entire pan-creas with the consistency of “red mud.” The gallbladder waspalpated with no evidence of stones.

Postoperatively octreotide given subcutaneously twice a daywas started. Stool and blood cultures obtained on admission andcultures of the pancreatic tissue grewSalmonella typhimuriumsensitive to ciprofloxacin. An echocardiogram performed torule out endocarditis was negative for vegetations. Intravenousciprofloxacin 400 mg every 12 hr was given for 21 days, fol-lowed by oral ciprofloxacin 500 mg twice a day for 7 days.Oral nutrition was started and TPN discontinued on the 13thand 20th postoperative days, respectively. Pancreatic enzymesupplementation was started postoperatinely. Clinical improve-ment continued and she was discharged on hospital day 31 onoctreotide 50µg subcutaneously twice a day and pancreaticenzymes.

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NECROTIZING ACUTE PANCREATITIS INDUCED BYSalmonella typhimurium

Fig 1. Axial enhanced computed tomogram through the pancreas showsan extensive nonencapsulated inflammatory process containing numer-ous small gas bubbles in devitalized nonenhancing portions of pancreatichead and body. Only a portion of the tail of the pancreas was spared.

DISCUSSION

Salmonellapancreatitis is a very rare clinical entity.Several studies have suggested thatSalmonellagastroen-teritis may be associated with an elevation of amylase or li-pase. Renner et al (1) reported elevated amylase and lipasein 62% (29 of 47) of patients, while Baert et al (2) reported23% (7 of 31) of patients with elevated lipase levels in pa-tients withSalmonellagastroenteritis. In all of these cases,however, the pancreatitis was either mild, with a Glasgowscore≤2 and/or minimal to moderate pancreatic enlarge-ment on abdominal ultrasound, or not clinically apparentat all. The majority of case reports involving salmonellapancreatitis showed relatively mild–moderate pancreatitisnot requiring surgical intervention (3). WhenSalmonelladoes cause pancreatitis or, rarely, abscess formation, it isusually associated with infections ofS. typhi(4, 5).

The etiology ofSalmonellapancreatitis is not clearlyunderstood. Hematogenous or lymphatic invasion hasbeen proposed. Direct invasion of the pancreas by the or-ganism has also been suggested (5). The biliary system hasbeen considered a portal of entry for seeding of the organ-ism asSalmonellathrive in bile rich medium (6). This maybe especially true in patients with predisposing conditionsto biliary stasis, such as cholelithiasis, choledocholithi-asis, and biliary duct abnormalities. Three case reportsof Salmonellainfection causing pancreatitis resulting insurgery support this. A 47-year-old woman hadS. typhirecovered from gallstones and pancreatic tissue (6). A

57-year-old male veterinary aide grewS. dublinin bloodculture and gallbladder. At laparotomy about 50 stoneswere removed in a mildly inflamed gallbladder (7). A35-year-old with an 11-cm pancreatic abscess grewS. typhimurium from the abscess, biliary drainage,and stool. The surgically removed gallbladder showedcholelithiasis and chronic cholecystitis (8).

This case illustrates that severe necrotizing pancreatitisassociated withSalmonellacan be seen without predis-posing biliary tract abnormalities. CT scan and surgeryrevealed a normal galbladder with no evidence of stones.Although this does not completely rule out a biliary originas the portal of entry for seeding, it makes other etiolo-gies more likely, such as a hematogenous or lymphaticinvasion.

The major findings in the pancreatic bed were the pres-ence of extensive gas and inflammatory mass without thepresence of visible fluid on CT scan. Use of the term ab-scess indicates the presence of infected fluid in a loculatedarea. An abscess may develop as part of the continuum ofnecrotizing pancreatitis; however, since no fluid collectionwas present in this case and the majority of the pancre-atic bed was necrotic tissue without abscess, as confirmedby surgery, the term necrotizing pancreatitis was moresuitable.

Additionally, as with other causes of infected necro-tizing pancreatitis, aggressive surgical management witheither debridement and continuous irrigation or frequentstaged debridements are the treatments of choice. Atsurgery there was gross necrosis of the pancreas in vir-tually the entire pancreatic bed. This likely accounted forthe normal amylase and lipase on admission. It was de-cided to perform surgery before a culture of pancreatictissue was obtained by fine-needle aspiration secondary tothe patient’s deteriorating clinical condition despite broad-spectrum parenteral antibiotics.

There has never been a proven role for octreotide inacute pancreatitis; however, it has been demonstrated thatoctreotide decreases pancreatic secretions in pancreaticfistulas. In this case with a near subtotal pancreatectomy,the output of the drain was consistent with pancreaticfistula and, theoretically, octreotide could promote fasterhealing if fistula output was reduced. Since there was nochange in output with octreotide, it was discontinued soonafter discharge with fistula closure several months later.

Since resection was done by removing nonviable tissue,not along classic anatomical planes, a portion of the tail re-mained. Since there would be no connection between themain pancreatic duct to the small bowel, pancreatic en-zyme supplementation was empirically given to preventmalabsorbtion. The patient maintained normal nonfast-ing glucose levels from postoperative day 7 though the

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remainder of the hospital stay. Thus the number of betacells that remained viable in the tail of the pancreas wassufficient to meet her endocrine needs.

REFERENCES

1. Renner F, Nimeth C, Demmelbauer N: High frequency of concomitantpancreatitis in salmonella enteritis. Lancet 337:1611 1991

2. Baert D, De Man M, Oosterbosch L, Duyck, MC, Van der Spek P,Lepoutre L: Infectious gastroenteritis: Are they all the same? ActaClin Belg 50:269–273, 1995

3. Sevastos N, Kolokotronis K, Papatheodoridis GV: Acute pancreatitisassociated withSalmonellaenteritidis. AJG, 96:3450–3451, 2001

4. Russell IJ, Forgacs P, Geraci JE: Pancreatitis complicating typhoidfever. Report of a case. JAMA 235:753–754, 1976

5. Hearne SE, Whigham TE, Brady CE: Pancreatitis and typhoid fever.Am J Med 86:471–473, 1989

6. Kune GA, Coster D: Typhoid Pancreatic Abscess. Med J Aust 1:417–418, 1972

7. Andren-Sandberg A, Hojer H: Necrotizing acute pancreatitis inducedby Salmonellainfection. Int J Pancreatol 5:229–230, 1994

8. Strand CL, Sanders LS:Salmonella typhimuriumpancreatic abscess:report of a case. Ann Surg 44:654–656, 1978

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