Surg Today (2008) 38:178–183DOI 10.1007/s00595-007-3593-6

Reprint requests to: A. SuzukiReceived: September 25, 2006 / Accepted: June 21, 2007

Colonic Fistula Associated with Severe Acute Pancreatitis: Report of Two Cases

ATSUSHI SUZUKI1, SHOHACHI SUZUKI

1, TAKANORI SAKAGUCHI1, KOSUKE OISHI

1, KAZUHIKO FUKUMOTO1,

SHIGEYASU OTA1, KEISUKE INABA

1, YASUO TAKEHARA2, HARUHIKO SUGIMURA

3, TAKASHI UCHIYAMA4,

and HIROYUKI KONNO1

1 Second Department of Surgery, 2 Department of Radiology, and 3 First Department of Pathology, Hamamatsu University School of Medicine, 1-20-1 Handayama, Hamamatsu 431-3192, Japan4 Department of Surgery, Kikugawa General Hospital, Kikugawa, Japan

AbstractColonic fi stula is a rare and potentially critical sequela of severe acute pancreatitis, which requires surgical treatment. We report two cases that were successfully treated by a colectomy for colonic fi stula associated with severe acute pancreatitis. Case 1 is a 71-year-old man infected with pseudocysts owing to severe acute pancreatitis that developed into a colonic fi stula as an early complication with a resulting pancreatic abscess. This patient underwent a left hemicolectomy, a trans-verse colostomy, and drainage of the pancreatic abscess. He has done well without recurrent disease for 35 months following surgery. Case 2 is a 58-year-old woman who had a past history of drainage during a laparotomy for a pancreatic abscess induced by endoscopic retro-grade cholangiopancreatography 10 years earlier. She was admitted to our hospital with left lateral abdominal pain and low-grade fever. Abdominal magnetic reso-nance imaging showed a retroperitoneal abscess and fi stula to the descending colon. She underwent a left hemicolectomy and drainage of the retroperitoneal abscess. She has remained symptom-free for 20 months following surgery. The colonic fi stula should therefore be recognized as a late complication during long-term follow-up as well as an early sequela associated with severe acute pancreatitis.

Key words Acute pancreatitis · Colonic fi stula · Pancre-atic pseudocyst · Pancreatic abscess · Endoscopic retro-grade cholangiopancreatography

Introduction

Infl ammation caused by severe acute pancreatitis has a potential to erode contiguous viscera, which may result

in the development of gastrointestinal fi stulas. Colonic involvement such as stenosis, necrosis, and fi stula is a rare sequela associated with severe acute pancreatitis, and a fatal outcome as a result of this critical complica-tion has been noted in some reports.1–3 Colonic compli-cations occur at a frequency of 1% in patients with acute pancreatitis.4,5 Among these complications, the exact frequency of colonic fi stula remains unknown and little information is available on colonic fi stula as a late complication associated with severe acute pancreatitis. We report two cases successfully treated with surgery for colonic fi stula associated with severe acute pancre-atitis and refer to the importance of a long-term follow-up after treating patients for severe acute pancreatitis.

Case Reports

Case 1

A 71-year-old man was admitted to an affi liated hospital with a chief complaint of upper abdominal pain and he was diagnosed to have severe acute pancreatitis by abdominal computed tomography (CT) in December 2003. Abdominal CT showed a diffuse enlargement of the pancreas with peripancreatic infl ammatory change and the presence of fl uid collection in the lesser sac and the left anterior pararenal space. The CT grade was judged to be grade E, showing two areas of peripancre-atic fl uid collection.6–8 Moreover, Ranson’s objective prognostic signs were positive for six parameters: age over 55 years, a blood glucose level >200 mg/dl, a serum lactate dehydrogenase level over 350 IU/l, a serum aspartate aminotransferase (AST) level over 250 IU/l on admission, an increase in the blood urea nitrogen level, and hypocalcemia during the initial 48 h of admis-sion.6,7 Continuous regional arterial infusion of a prote-ase inhibitor (gabexate mesilate, Ono Pharmaceutical, Osaka, Japan) and antibiotics (Imipenem, Banyu

A. Suzuki et al.: Colonic Fistula Associated with Pancreatitis 179

Pharmaceutical, Tokyo, Japan) via gastroduodenal and splenic arteries was performed for 5 days for the man-agement of acute pancreatitis. Moreover, he underwent hemodialysis for 3 days because of pancreatitis-related acute renal failure. Oral intake was permitted 25 days after his admission with an improvement of his clinical symptoms and laboratory data, but abdominal CT in February 2004 showed pancreatic pseudocysts (Fig. 1A, B). Pyrexia occurred in March 2004 and percutaneous drainage was performed under a diagnosis of infected pancreatic pseudocyst. Drainage tubography revealed the presence of a colonic fi stula into the descending colon. Discharge from this cystic lesion comprised puru-lent matter and liquid feces with a smell. He was admit-ted to our hospital in May 2004 for the treatment of persistent pyrexia resulting from pancreatic abscess with a colonic fi stula.

The laboratory data on admission showed the pres-ence of anemia, infl ammatory fi ndings, liver dysfunc-tion, hypoalbuminemia, and coagulopathy as follows: hemoglobin 6.5 g/dl, white blood cell count (WBC) 6600 /mm3, platelet count 29.9 /mm3, C-reactive protein 4.72 mg/dl, total bilirubin 0.5 mg/dl, AST 104 IU/l, alanine aminotransferase 117 IU/l, alkaline phosphatase 1634 IU/l, amylase 41 IU/l, albumin 1.9 g/dl, and pro-thrombin activity 77%. Drainage tubography showed a negligible fi stula to the third portion of the duodenum as well as colonic fi stula to the descending colon (Fig. 1C, D).

Subsequently, both pancreatic abscess fl uid and blood cultures showed the presence of Escherichia coli, Enterococcus faecalis, Morganella morganii, and Proteus vulgaris. His condition was refractory to con-servative treatment, and we therefore performed a laparotomy in June 2004. Severe infl ammatory change with purulent ascites was observed from the left half of the transverse colon to the descending colon. After mobilization of the descending colon, we confi rmed the presence of a colonic fi stula at the splenic fl exure. In addition to the removal of necrotic material in the pancreatic abscess and pancreatic abscess drainage, a left hemicolectomy was performed with the construc-tion of a transverse colostomy and a jejunostomy for postoperative enteral nutrition. The resected speci-men had a fi stula with hemorrhagic necrosis penetrat-ing the tunica muscularis of the descending colon (Fig. 2A, B). Histologically, the so-called pericolitis, infl am-matory granulation tissue and infl ammatory cell infi l-tration, was observed on the colonic wall.4 No thrombosis was seen in the marginal artery of the colon (Fig. 2C).

The fi stula to the duodenum was not observed by drainage tubography 19 days following surgery. The purulent discharge from the pancreatic abscess gradu-ally decreased, with the disappearance of pyrexia by repeat lavage through the drainage tube. He left our hospital 64 days following surgery with an improvement in his general condition. He has done well without

Fig. 1. Contrast-enhanced computed tomography showing expansile pancre-atic pseudocysts (A) replacing the anterior pararenal space (B). Normal pancreatic parenchyma is scarcely visual-ized. Fistulography via an abscess drain-age tube showing a negligible fi stula (arrow) affecting the third portion of the duodenum (C) as well as a colonic fi stula communicating with the lumen of the descending colon (D)

180 A. Suzuki et al.: Colonic Fistula Associated with Pancreatitis

recurrent disease and pyrexia for 35 months following surgery.

Case 2

A 58-year-old woman was admitted to our hospital in July 2005 with a chief complaint of lumbago in the left back and pyrexia. Laboratory data on her admission were within normal ranges, except for WBC (9500 /mm3) and C-reactive protein (5.8 mg/dl). Abdominal magnetic resonance (MR) imaging showed the presence of abnormal gas in the retroperitoneal space adjacent to the spleen (Fig. 3A) and a fi stulous structure between this retroperitoneal lesion and the splenic fl exure of the

descending colon (Fig. 3B–D). No abnormal fi ndings were seen in the main pancreatic duct or biliary tract on MR cholangiopancreatography. Although an enema examination using gastrografi n and colonoscopy showed stenosis at the splenic fl exure of the descending colon, no fi stula was confi rmed except for an edematous mucosa during these examinations. The infl ammatory fi ndings temporarily normalized under water intake alone and the intravenous administration of antibiotics, but a low-grade fever and left lumbago appeared again after normal diet resumption. Subsequently, pyrexia developed in accordance with defecation.

This patient has a past history of a pancreatic abscess of about 10 years. In August 1995, she underwent

Fig. 2. The resected specimen, revealing the presence of a fi stula (A) with hemor-rhagic necrosis penetrating the tunica muscularis of the descending colon (B). Histological fi ndings showing the so-called pericolitis, infl ammatory granula-tion tissue and infl ammatory cell infi ltration, on the colonic wall adjacent to the fi stula (arrow, C) (H&E stain, ×5)

Fig. 3. Contrast-enhanced axial T1-weighted magnetic reso-nance image, revealing a recurrent retroperitoneal abscess (arrowheads) containing gas bubbles adjacent to the spleen (A), and a well-enhanced funicular structure (arrow) extend-

ing from the some signal voids caused by the retroperiton-eal abscess (B, C) to the splenic fl exure of the descending colon (D)

A. Suzuki et al.: Colonic Fistula Associated with Pancreatitis 181

endoscopic retrograde cholangiopancreatography (ERCP) as a careful follow-up for cholecystolithiasis. She complained of upper abdominal pain following ERCP, and her serum amylase level showed a markedly high value (5540 IU/l). The abdominal CT on day 2 fol-lowing ERCP showed fl uid collection around the pan-creas and pleural effusion. Her illness was diagnosed to be severe acute pancreatitis induced by ERCP. The severity of acute pancreatitis by CT grading was judged to be grade E with two or more areas of peripancreatic fl uid collection.6–8 The intravenous administration of a protease inhibitor (gabexate mesilate) and antibiotics had been performed for 2 weeks. Although oral intake was permitted because of the improvement of clinical symptoms, pyrexia occurred 2 weeks after diet resump-tion. The presence of an abscess extending from the pancreatic body to the tail with a small amount of gas was confi rmed by abdominal CT. She underwent a cho-lecystectomy and pancreatic abscess drainage during a laparotomy in September 1995, and was discharged from our hospital 3 months following surgery with a disappearance of the pancreatic abscess. She has since remained symptom-free for 10 years.

From the fi ndings of her medical imaging and clinical course, including her past history, we considered that her symptoms had most likely arisen from a colonic fi stula connection between the retroperitoneal abscess and the descending colon.

A laparotomy was performed in September 2005. The colonic wall contiguous to the splenic fl exure was very thick with infl ammatory changes, and hard fi stulous structures connecting to the retroperitoneal abscess were observed after the mobilization of the splenic fl exure. A left hemicolectomy was performed with end-

to-end anastomosis and abscess drainage. Macroscopi-cally, two fi stulous structures were seen in the resected specimen (Fig. 4A). Histologically, two fi stulae were identifi ed in the layers of the mucosa and the tunica muscularis of the descending colon at the splenic fl exure, which were surrounded by infl ammatory cells and gran-ulation tissue (Fig. 4B, C). There were no fi ndings of either thrombosis or typical pericolitis.

The postoperative course was uneventful with an improvement in her symptoms. She was discharged 24 days following surgery and has remained well for 20 months without either recurrent disease or any complaints.

Discussion

Severe acute pancreatitis has a potential to involve con-tiguous organs, such as the colon, stomach, and duode-num. The peritoneal refl ections from the anterior surface of the pancreas provide a route for the spread of extensive peripancreatic exudates including pancre-atic enzymes and infl ammatory mediators within the transverse mesocolon and the small bowel mesentery.1 The splenic fl exure is in close proximity to the pancre-atic tail and acute pancreatitis with infected pseudocysts at the pancreatic tail thus spreads to the splenic fl exure. As a result, pericolonic infl ammation may act as a caus-ative factor of colonic fi stula.

Colonic complications have been generally consid-ered rare in acute pancreatitis,4,5 but the frequency of this serious morbidity is increased with the severity of acute pancreatitis.9–14 In the English literature, colonic involvement and colonic perforation or fi stula has been

Fig. 4. A resected specimen showing two fi stulas (arrow, A). A loupe image reveal-ing the thinning of the colonic wall around the site of the fi stula and kink of all layers of the colon (B). Histopathological exam-ination revealing the fi stula surrounded by infl ammatory cells and granulation tissue without fi ndings of typical pericoli-tis (C). (H&E stain, ×25)

182 A. Suzuki et al.: Colonic Fistula Associated with Pancreatitis

observed in 15%–27% and 3%–10% of patients with severe acute pancreatitis treated with surgery, respec-tively9–11,14 (Table 1). The outcome following surgery for colonic fi stula in patients with severe acute pancreatitis showed a high mortality rate ranging from 17%–67% (Table 1). This result may depend on the extent of severe acute pancreatitis.

Colonic fi stula may occur as an outcome of an enlarged mass exerting pressure, such as a pancreatic abscess or pseudocyst, draining into the colon. Negro and associates15 indicated that colonic fi stula developed within a period ranging from 10 days to 90 days after the onset of acute pancreatitis. In Case 1, colonic fi stula was observed 53 days after the recurrence of acute pancreatitis with a protracted course, despite intensive support therapy. In contrast, colonic fi stula in Case 2 was not accompanied with either a pancreatic abscess or pseudocyst, unlike Case 1. Pancreatic fi stula has been seen in patients with chronic pancreatitis12 but there has been no case report indicating colonic fi stula develop-ment occurring around 10 years after treatment for pan-creatic abscess or pancreatic pseudocyst, as observed in Case 2. Taking the histological fi ndings of the resected specimen into consideration, the pathogenesis in Case 2 may have been different from that in Case 1 with pericolitis. Although the precise mechanism of colonic fi stula in Case 2 remains unknown, the presence of retained infl ammation at the left infraphrenic space might have been associated with the formation of colonic fi stula as a late complication around 10 years after the treatment for pancreatic abscess or pancreatic pseudocyst. Attention should therefore be paid to the occurrence of colonic fi stula over a long-term period in patients with exacerbation of the disease irrespective of aggressive medical treatment for severe acute pancreatitis.

Because colonic perforation or fi stula is complicated by persistent or spontaneous infection, or overwhelm-ing sepsis, surgical treatment is usually required to cure

this critical complication. Although a recent case report has described colonic fi stula successfully managed by endoscopic therapy,16 little information is available regarding as to which patients are appropriate for this treatment. Regarding surgical procedures, there are two types of surgical strategies: a diverting ileostomy with the preservation of the large bowel, and a resection of the responsible segment of the colon (Table 1). The colonic fi stula in our cases was suitably managed with the surgical removal of the responsible segment, but surgical procedures should be selected according to the degree of infl ammation and/or patient condition. Con-sequently, our two cases have survived for 35 and 20 months following surgery without recurrent disease.

In conclusion, the two cases with colonic fi stula asso-ciated with severe acute pancreatitis were successfully treated with a resection of the involved colon. Because this complication was observed 10 years after the surgi-cal drainage of a pancreatic abscess, attention should thus be paid to the occurrence of colonic fi stula over a long-term period in patients with a history of medical treatment for severe acute pancreatitis.

References

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3. van den Biezenbos AR, Kruyt PM, Bosscha K, van Leeuwen MS, Feldberg MA, van der Schouw YT, et al. Added value of CT cri-teria compared to the clinical SAP score in patients with acute pancreatitis. Abdom Imaging 1998;23:622–6.

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Table 1. A review of the English literature reporting colonic fi stula induced by severe acute pancreatitis

First authorRef. No. of SAP

No. of colonic

Treatment of colonic fi stula Mortalitycomplications fi stula

Kriwanek9 71 14 (20%) 5 (7%) Diverting ileostomy in 2a 3/5 (60%)Ho10 118 NR 12 (10%) Diverting ileostomy in 2

Diverting colostomy in 10b2/12 (17%)

Bouillot11 100 15 (15%) 3 (3%) Suture of colonic fi stula in 1Colostomy followed by colectomy in 1Colectomy with anastomosis in 1

2/3 (67%)

Van Minnen14 59 16 (27%) 7 (7%) Colectomy in 4 NR

SAP, severe acute pancreatitis treated with surgery; NR, not reporteda A discontinuity resection was performed 5 days and 12 days after ileostomyb Subsequent fi stula resection and colostomy closure were performed in four patients

A. Suzuki et al.: Colonic Fistula Associated with Pancreatitis 183

7. Ranson JHC. Acute pancreatitis: surgical management. In: Go VLW, DiMango EP, Gardner JD, Lebenthal E, Reber HA, Scheele GA, editors. The pancreas: biology, pathobiology and disease. 2nd ed. New York: Raven; 1993. p. 637–48.

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14. Van Minnen LP, Besselink MGH, Bosscha K, Van Leeuwen MS, Schiper MEI, Gooszen HG. Colonic involvement in acute pancreatitis: a retrospective study of 16 patients. Dig Surg 2004;21:33–8.

15. Negro P, D’Amore L, Flati G, Gossetti F, Guadagni S, De Ber-nardinis G, et al. Colonic involvement in pancreatitis: six cases more. Int Surg 1991;76:122–6.

16. Howell DA, Dy RM, Gerstein WH, Hanson BL, Biber BP. Infected pancreatic pseudocysts with colonic fi stula formation successfully managed by endoscopic drainage alone: report of two cases. Am J Gastroenterol 2000;95:1821–3.