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Q1: What is the endoscopic diagnosis (see fig 1 on p243)?
Haemobilia. Bile and blood are seen trickling through the end-on ampulla. Upper gastrointestinal endoscopy was done twice, within 24 hours of the first and the second bleed, and was normal on both occasions, thereby indicating intermittent bleed from the biliary tract.
Q2: What is the procedure and what does it show (see fig 2 on p244)?
The procedure is hepatic angiography and shows two large lobulated pseudoaneurysms in the right lobe of the liver supplied by a single branch of the right hepatic artery (fig 2A). Superselective catheterisation of the feeding branch and embolisation were done using two coils (3 cm × 4 mm). Postembolisation angiography shows complete cut off of the pseudoaneurysm with block of the feeding artery (fig 2B). The patient was asymptomatic after the procedure.
Sandblom and Mirkovitch described hepatic artery pseudoaneurysm formation as a complication after blunt or a penetrating trauma to the liver or after a percutaneous diagnostic or therapeutic procedure performed on the hepatobiliary system and presenting as haemobilia.1 A meta-analysis on a Medline search showed that two thirds of cases of haemobilia were iatrogenic, while accidental trauma accounted for 5% of the cases.2 Croce et al reviewed surgery details of 482 patients with hepatic injury.3 Six developed haemobilia, three were due to blunt trauma (1.2%). Based on the hepatic injury scale the present case had grade III type of hepatic artery injury.4
The formation of intrahepatic cavity of blood and bile after blunt injury to the liver can predispose the patient to develop hepatic artery aneurysm.1
In an experimental study, Sandblom and Mirkovitch showed that bile retards liver healing and causes lysis of clotted blood.1 This could result in an unrecognised arterial injury leading to a pseudoaneurysm; infection contributes further to its development. As the cavity expands due to continued bleeding at arterial pressure, progressive pressure necrosis develops around the margin. Also the poor contractility of the vessels results in a persistent haemorrhage into the cavity. The cavity eventually erodes into a major branch of the biliary tree, which is already damaged by either the initial injury or the interventional procedure, thus resulting in haemobilia.
Diagnosis of haemobilia is based on the Quincke’s triad: jaundice (51%), colicky abdominal pain (80%), and blood in either vomitus or stool (62%). The bleed may be a major one and life threatening or minor. It can present several weeks after injury. Duodenoscopy can image blood oozing from the papilla of Vater as was possible in our case. Endoscopic retrograde cholangiopancreaticography may show biliary tracts filled with blood clots. Ultrasound can detect intrahepatic haematomas and arterial aneurysms. Both these procedures were useful in diagnosis in the present case. Abdominal computed tomography and selective visceral angiography, apart from showing the site of bleed, can also help in detecting arterial variations.5 Long standing haemobilia is associated with rapidly developing intrahepatic collaterals. Superselective catheterisation may be necessary.
Management is aimed at tackling the pseudoaneurysm, the intrahepatic cavity,3 and relieving the biliary obstruction. Selective arterial embolisation of the pseudoaneurysm is the procedure of choice. Surgery is reserved for those refractory to embolisation. Green et al managed 43% of patients with haemobilia conservatively and 36% by transarterial embolisation.2 The mortality rate was 5%. Large cavities (8 cm and above) after blunt trauma would require debridement since they act as sources of infection. Occasionally, the debridement can stop the bleed and also result in regression of small hepatic cavity (2 × 2 cm).3
The clinical presentation of haemobilia, which was distinct in the present case, was confirmed at duodenoscopy. Transarterial embolisation controlled the bleed.
Haemobilia caused by blunt trauma.