Br. J. Surg. Vol. 67 (1980) 42-30 Printed in Great Britain

Pancreatic pseudocyst with gastric and colonic connections treated conservatively S A N D R A D E A N , M A R T I N J . K E N D A L L A N D G E O F F R E Y S L A N E Y *

SUM MARY A case of pancreatic pseudocysr with gastric and colonic connections developing after acute pancreatitis is re- ported. The successful treatment by conservative means is described and alternative methods of management are revie wed.

PANCREATIC pseudocyst formation complicates about 2 per cent of cases of acute pancreatitis ( I ) . Of these approximately 5 per cent rupture, usually into the gastrointestinal tract, the peritoneum or the pleural cavity (2). Rupture into more than one hollow viscus is rare.

When fistulous connections form between the colon and a pancreatic pseudocyst there is a serious risk of the patient dying either from haemorrhage or infection (3). To prevent these complications the suggested scheme of management has been careful investigation to delineate the problem followed by early laparotomy, drainage and proximal colostomy (3,4). The patient we report here is of interest because she developed at least two spontaneous fistulous connections with the gastro- intestinal tract, and although the colonic fistula bled, it settled spontaneously without surgical intervention.

Case report A 67-year-old housewife was admitted with a 6-week history of anorexia, 12.5 kg weight loss, occasional bile-stained vomiting and intermittent melaena. There was no history of aspirin ingestion, alcohol abuse or smoking and her only medication was Triptafen (amitriptyline) taken for chronic depression. Two months previously, whilst on holiday, she had been admitted to another hospital complaining of severe abdominal pain. A diagnosis of acute pancreatitis was made and con- firmed by an elevated serum amylase. She was treated with intravenous fluids, analgesics and antibiotics. She responded satisfactorily and was discharged on a low fat diet. On admission to this hospital she appeared to be clinically

anaemic, depressed and wasted. There was an apical systolic murmur and bilateral ankle oedema. In the epigastrium there was a soft, ill-defined mass with transmitted pulsation.

Her haemoglobin was 9.8 g/dl with a hypochromic micro- cytic picture and her ESR was 61 mm in the first hour. The only abnormalities in her biochemical profile were a low albumin (22 g/l) with a correspondingly low calcium (2.13 mmol/l) and a marginally raised aspartate transferase (44 units/]). A straight X-ray of the abdomen did not show any opaque biliary calculi. Faecal occult blood tests were positive on three occasions. Sipoidoscopy was normal. A barium meal showed a mass in the region of the lesser sac containing some gas bubbles, into which a small quantity of barium was leaking from a fistula arising from the posterior portion of the gastric antrum (Fig. 1). A barium enema demonstrated that there was also a fistulous connection from the transverse colon to the same 'abscess cavity' (Figs. 2, 3). In view of the serious risk of haemorrhage and infection, laparotomy was anticipated and the patient was given antibiotics, a blood transfusion and albumin. However, these measures produced such a gratifying improvement that the operation was postponed. Improvement continued and the upper abdominal mass subsided spontaneously.

Fig. 1. Barium meal showing gas bubbles in the lesser sac and barium leaking from the posterior portion of the gastric antrum.

One year later the patient remains well with a normal haemoglobin and a repeat barium enema examination shows no evidence of a fistula or of a mass in the region of the lesser sac.

Discussion The development of a fistula from a pancreatic pseudocyst should be suspected in a patient who has the triad of protracted pancreatitis, an upper abdominal mass and evidence of blood loss in the faeces (3).

The aetiology of fistula formation following acute pancreatitis remains obscure. Although chemical injury by pancreatic trypsinogen activated by colonic entero- kinase may occur, it is unlikely to be the sole cause as fistula formation is a late complication of acute pancreatitis (6). Corlette and Lynch (7) offer an alterna- tive explanation and suggest that pressure from an enlarging inflammatory mass together with bacterial digestion may cause the erosion, just as any abscess may rupture into adjacent viscera. They consider that a less likely cause is thrombosis in the colonic venous drainage. However, this is a possibility, since colonic

* S. Dean and M. J. Kendall, Department of Clinical Pharmacology, G. Slaney, Department of Surgery, Queen Elizabeth Hospital, Birmingham. Correspondence to: M. J. Kendall.

430 S. Dean et al.

Fig. 2. Barium enema showing leakage through the fistula (arrowed).

gangrene is known to occur in pancreatitis associated with occlusion of the portal system (8).

The literature suggests that the risk of bleeding is so great as to make pancreaticocolic fistula an indica- tion for urgent surgical intervention. However, some patients have recovered with conservative management (5). Thus, the clinician faced with a patient with this complication may be in a dilemma regarding the best course of action.

Our experience suggests that, provided that the patient is carefully observed and adequate blood is available, non-surgical measures may suffice to allow spontaneous healing. The conservative management should include nasogastric suction, intravenous fluids and blood if necessary, together with appropriate antibacterial therapy such as gentamicin and metronidazole-effective against colonic organisms in- cluding the anaerobes. In addition, it may be necessary to maintain the patient’s nutrition by intravenous feeding.

Acknowledgements We thank Alan Wilkinson for his help in the management of this case.

Fig. 3. Barium enema showing a large cavity extending from the fistula (bottom arrow) upwards and to the left (top arrow).

References 1. ROSENBERG I . K . , KAHN J . s. and WALT A . J.: Surgical

experience with pancreatic pseudocysts. Am. J . Surg. 1969;

2. SHATNEY c. H . and SOSIN H.: Spontaneous perforation of a pancreatic pseudocyst into the colon and duodenum. Am. J. Surg. 1973; 126: 433-8.

3. BERNE T. v. and EDMONDSON J . A,: Colonic fistulation due to pancreatitis. Am. J. Surg. 1966; 111: 359-63.

4. I~OHLMAN T. w., KATON R. M., LEE T. G. et al.: Use of the endoscopic retrograde cholangiopancreatography in the diagnosis of pancreatic fistula. Gastroenterology 1976; 70:

117: 11-17.

582-4.

119 200-7. 5. JORDAN G . L. JUN.: Pancreatic fistula. Am. J . SUrg. 1970;

6. GATCH w. D. and BRICKLEY R . A, : Perforation of the colon following acute necrosis of the pancreas-3 cases. Arch. Surg. 1951; 63: 698-701.

7. CORLETTE M. B. and LYNCH J . A, : Pancreatitis presenting as a colonic fistula. Arch. Surg. 1972; 104: 708-9.

8. HOWARD J . M. and JORDAN G. L.: Surgical Diseases of the Pancreas. Philadelphia: Lippincott, 1960.

Paper accepted 12 November 1 9 7 9 .