Liver abscess is a serious complication following TACE and RFA. It often results in a prolonged hospital stay and can be fatal [1
]. The reported incidence of liver abscess following TACE is between 0.3% and 2.7% [4
] and, following RFA, between 0.66% and 2.4% [6
]. A major risk factor for liver abscess formation following TACE and RFA is the presence of abnormal bilio-enteric communications (e.g.
surgical bilio-enteric reconstructions) or a functionally incompetent sphincter of Oddi (secondary to sphincterotomy or biliary-enteric stent/drain) [1
]. In the presence of a bilio-enteric anastomosis, the risk of liver abscess formation is increased up to 800 times (odds ratio of 894) following TACE and 36 times (odds ratio of 36.4) following RFA [1
]. The increased risk related to these procedures is believed to be due to ascending bacterial colonisation of the biliary tree by enteric flora through an incompetent sphincter of Oddi or retrograde colonisation in the case of bilio-enteric anastomoses. A biliary tree colonised by enteric bacteria predisposes the ablated necrotic liver or tumour tissue to secondary infection, with locoregional ischaemia induced by TACE and RFA contributing to the risk.
Many operators consider the presence of a bacterial colonised biliary tree to be a contra-indication for TACE and RFA because of the significant increase in risk of septic complications. Several strategies, including prolonged antibiotics coverage and cleansing enemas, are being developed for this group of patients, with varying success [8
]. The diagnosis of liver abscess formation following TACE and RFA is a challenge. An abscess can form 1–4 weeks after TACE. If symptoms occur in the period immediately following TACE, it can be difficult to distinguish it from post-embolisation syndrome. Furthermore, the presence of air at the site of TACE and RFA is not an uncommon imaging finding and has been shown not to be specific for abscess formation [9
]. Therefore, the diagnosis of abscess formation after TACE and RFA remains largely clinical. This diagnostic challenge forms the rationale for prolonged antibiotics therapy (4–6 weeks) in suspected or high-risk cases and underscores the need for vigilance in identifying patients at risk.
Spontaneous cholecysto-enteric fistula formation is a rare complication of choledocholithiasis. Cholecysto-duodenal fistula followed by cholecystocolic fistula are more common [10
]. The fistulous communication is formed along the track of the gallstones as they erode through the inflamed gallbladder into the adjacent bowel.
Cholecysto-enteric fistula is a diagnostic challenge. It is often clinically silent and subtle on imaging [10
]. As illustrated in our case, the patient was asymptomatic and the tell-tale signs (e.g.
aerobilia) can be minimal. However, we believe a mature bilio-enteric fistula poses the same risk for abscess formation after TACE and RFA. The fistula serves as a conduit for ascending bacteria colonisation of the biliary tree in the same way as its iatrogenic counterparts. Enteric flora is commonly isolated from post-TACE or RFA liver abscesses [1
]. Aspiration of the abscess in our case would have allowed further antimicrobial study, especially when the colonising bacteria is likely to be of colonic origin as opposed to small bowel origin in all previously reported cases. However, aspiration was not required as the patient responded well with conservative treatment.
Prior to TACE and RFA, relevant history of previous biliary interventions and imaging findings of aerobilia or biliary stents/drains allows easy identification of high-risk patients. In contrast, owing to its innocuous and silent nature, detection of a spontaneous bilio-enteric fistula requires rigorous review of pre-procedural imaging, particularly in patients with gallstone disease.