Omental and extraperitoneal abscesses complicating cholecystocolic fistula

Abstract

Background

Acute cholecystitis resolves with conservative treatment in most patients, but empyema or perforation of an ischaemic area may develop, resulting in a pericholecystic abscess, bile peritonitis or a cholecysto-enteric fistula.

Case outline

A 63-year-old man presented with extraperitoneal and omental abscess formation complicating a cholecystocolic fistula secondary to gallbladder disease. Histological examination of the gallbladder and omentum showed xanthogranulomatous inflammation.

Conclusion

A detailed literature review failed to demonstrate a previous report of this combination of rare complications of gallbladder disease.

Introduction

Xanthogranulomatous cholecystitis is associated with a high incidence of complications including biliary-enteric fistula, which is a rare complication of gallbladder disease. The diagnosis of biliary-enteric fistula can be delayed because of lack of a specific clinical picture, which can lead to development of further complications ¹. We describe the management of a patient who developed omental and extraperitoneal abscesses secondary to cholecystocolic fistula.

Case study

A 63-year-old man was admitted with a 4-week history of upper abdominal pain associated with weight loss of 16 kg over the previous 2 months. There was a long history of chronic dyspepsia, plus bronchial asthma, ischaemic heart disease, severe rheumatoid arthritis and hypertrophic obstructive cardiomyopathy. He had previously undergone left total hip replacement and appendicectomy.

On examination the patient was pale, apyrexial, normotensive, tachycardic (130/min) but without any signs of heart failure. Abdominal examination revealed a palpable tender epigastric mass measuring 9×8 cm. Investigations showed a normal haemoglobin (12.3 g/dl; 1.9mmol/L), but raised white cell count (20.2×10⁹), erythrocyte sedimentation rate (110 mm/h) and Creactive protein (229 mg/L). Liver function tests, coagulation screen, serum amylase, urea, creatinine and electrolytes were all within the normal range. Abdominal and chest X-rays were normal. Abdominal ultrasound showed a distended gallbladder but no evidence of active inflammation or stones. Computed tomography (CT) of the abdomen demonstrated an 8×10-cm mass lesion in the midline between the transverse colon and anterior abdominal wall in the upper abdomen (Figure 1). Barium enema revealed indentation and narrowing of the distal transverse colon by the large upper abdominal mass with some mucosal irregularities. Barium meal and gastroscopy were normal. An echocardiogram showed a dilated left atrium, mitral valvular incompetence and hypertrophic obstructive cardiomyopathy. Cardiac catheterisation and coronary angiography excluded serious coronary artery disease. The patient developed spiking fever up to 38 °C with persistently elevated white blood cell count and inflammatory markers, and a clinical diagnosis of an abscess was made. Repeat abdominal CT with a view to percutaneous fine-needle aspiration showed that the previously identified mass lesion had broken down with fistulation between transverse colon and gallbladder via the anterior abdominal wall, in keeping with cholecystocolic fistula (Figure 2). He was treated with intravenous antibiotics (piperacillin-tazobactam) to control systemic sepsis. After successful treatment of septicaemia and preoperative bowel preparation, laparotomy revealed a large abscess within the omentum, which was communicating with another abscess cavity lying extraperitoneally just behind the anterior abdominal wall. There was a fistulous tract from the fundus of the gallbladder to the transverse colon. The gallbladder was thick-walled and chronically inflamed. Part of the greater omentum containing the abscess was excised. Cholecystectomy was performed, with excision of the fistula and closure of the defect in the transverse colon. Intra-operative cholangiogram was normal. The patient made an uneventful postoperative recovery and was discharged home on the 8th postoperative day.

Figure 1. .

CT scan of upper abdomen showing an 8×10-cm mass lesion between transverse colon and anterior abdominal wall.

Figure 2. .

Repeat CT scan of upper abdomen showing that the previously identified mass lesion has broken down with communication with the transverse colon.

Histological examination of the gallbladder showed xanthogranulomatous cholecystitis. The omental tissue showed extensive fibrosis surrounding foci of xanthogranulomatous inflammation and fat necrosis.

Discussion

Biliary-enteric fistulas comprise <1% of all biliary disorders and may form between any part of the extra-hepatic biliary tree and an adjacent portion of the gastrointestinal tract ². The commonest type of biliary-enteric fistula is cholecystoduodenal (70%), followed by cholecystocolic (14%), cholecystogastric (6%) and choledochoduodenal (4%) ³. Multiple fistulas occur in approximately 2% of cases ⁴.

Causes of spontaneous biliary-enteric fistulas are biliary tract disease (90%), peptic ulcer disease (6%) and other rare causes including inflammatory bowel disease, trauma, pancreatitis and malignancy (4%) ⁵. Patients with biliary-enteric fistula may have a long history of biliary tract disease and a clinical picture similar to that of chronic calculous cholecystitis ². In this group of patients, the fistula is usually found during cholecystectomy, where the gallbladder is small, fibrotic and adherent to other viscera ². On the other hand, biliary-enteric fistula may be overshadowed by other more dramatic manifestations of biliary tract disease such as acute cholecystitis, cholangitis, pancreatitis or intestinal obstruction due to gallstone ileus ¹,². Cholecystocolic fistula can cause severe diarrhoea ⁶. The diagnosis of biliary-enteric fistula is suggested by air in the biliary tree, which is present in as many as 50% of patients ⁵. Barium studies may demonstrate the passage of contrast into the biliary tree. If the cystic duct is obstructed, the gallbladder and fistula will not be visualised by ERCP. Nuclear biliary scintigraphy may delineate the fistula but false-positive and false-negative studies have been reported.

General principles of treatment are: to establish the anatomy and cause of the fistula, control infection, eliminate underlying biliary obstruction, correct electrolyte abnormalities and operate after bowel preparation ⁷. The surgical treatment of choice of biliary-enteric fistula is cholecystectomy, disconnection of the fistula and closure of the bowel ⁶.

Intra-operative cholangiography is recommended to outline the anatomy of the biliary tree ¹. Cholecystocolic fistula has recently been treated successfully by laparoscopy ¹.

Biliary-enteric fistulas may be associated with severe systemic sepsis due to contamination of the biliary tract with mixed colonic bacteria. This problem should be treated early with intravenous antibiotics to prevent septic shock; the antibiotic used should cover gram-positive, gram-negative and anaerobic organisms.

Omental abscess has not been previously reported as a complication of cholecystocolic fistula or gallbladder disease, except as a postoperative complication following loss of stones into the peritoneal cavity during cholecystectomy ⁸. Primary abscesses of the greater omentum have also been described ⁹,¹⁰,¹¹,¹².

Xanthogranulomatous cholecystitis (XGC) is a focal or diffuse destructive inflammatory process of the gallbladder ¹³. The incidence of XGC in gallbladder disease ranges from 5 to 13% ¹⁴,¹⁵. It can result from obstruction of bile flow, plus infection with leakage of bile into the gallbladder wall. Histiocytes then phagocytose bile pigments, haemosiderin and cholesterol, resulting in the formation of xanthoma cells ¹³. Macroscopically the gallbladder is characterised by yellowish tumour-like masses in its wall with a tendency to adhere to adjacent tissues, which can give rise to the suspicion of malignancy at operation ¹⁶.

Microscopically XGC is characterised by varying degrees of acute and chronic inflammatory cell infiltration, as well as many macrophages containing lipid (foamy histiocytes, xanthoma cells). The condition is very difficult to distinguish clinically from other forms of gallbladder inflammation, and a malignant neoplasm can be suggested either on ultrasound or CT scan. The operative appearances of a thickened and adherent gallbladder can be worrying. XCG has a high frequency of complications such as perforation, abscess and fistula formation ¹⁷.