A 75-year-old male patient with alcoholic cirrhosis and portal hypertension, abstinent for 6 years. Routine imaging detected a 38mm lesion on segment IVa, suggestive of hepatocellular carcinoma (HCC) with afferent vascularisation originating in the middle hepatic artery (MHA). Multidisciplinary consensus decided drug-eluting bead trans-arterial chemoembolisation (DEB-TACE) as first line treatment.
First DEB-TACE was successful and uneventful. Nevertheless, 1-month control CT demonstrated partial response (Fig. 1).
At the second DEB-TACE, two suspicious areas were detected (Fig. 2). The first area matched the known viable tumour and was successful retreated with DEB-TACE.
During manual contrast injection at the afferent vessel of the second area, there was atypical contrast reflux and a blush thought to correspond to arterial perforation and active bleeding (Fig. 3). The microcatheter was pulled downstream, but no abnormalities were seen in the following angiograms (Fig. 4).
It was concluded that an arterio-biliary fistula had been created, resulting in opacification of the biliary tract, including the cystic duct and the gallbladder. Contrast stasis in the gallbladder lumen was seen in the following series and at cone-beam CT (Fig. 5). Despite apparent spontaneous resolution, embolisation with polyvinyl alcohol (PVA) particles was performed to ensure fistula treatment.
Arterio-biliary fistulas are rare, with the most common cause being liver biopsy, although it is estimated to happen in less than 1% of biopsies . It has also been described after biliary lithiasis and infection, blunt liver trauma, tumour necrosis, arterial pseudoaneurysm and other hepatobiliary interventions, such as surgery, percutaneous cholangiography, endo-biliary prosthesis and abscess drainage [2-4].
Typical signs and symptoms include right-upper quadrant pain, jaundice and upper gastrointestinal haemorrhage (haematemesis or melena) [2-4].
Endovascular procedures are the treatment of choice following intrahepatic, arteriovenous, portosystemic and arterio-biliary fistula. Therapeutic options include the use of coils, PVA or histoacryl glue [5-7].
In our particular case, the patient did not develop any signs or symptoms, and the arterio-biliary fistula was quickly and spontaneous resolved, with no further opacification of the biliary tract in the following angiograms. Embolisation with PVA particles was still performed to ensure fistula treatment (Fig. 2). This area was not further embolised with drug-eluting beads due to the risk of biliopathy. No special imaging follow-up was advised, further than the regular 1-month CT control after DEB-TACE.
We hypothesise that there was an increased tissue susceptibility due to tumour growth and neovascularisation. This facilitated the disruption of the arterio-biliary barrier during supraselectivation and wedging of the microguidewire of the subsegmental artery involved, and the ensuing manual contrast injection.
In conclusion, although rare, arterio-biliary fistula can be a potential complication of endovascular liver procedures, and should be promptly diagnosed and treated.
Written informed patient consent for publication has been obtained.
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