Hepatic artery aneurysms (HAA) are rare and represent 20% of all visceral artery aneurysms, the commonest being splenic, second commonest hepatic, followed by superior mesenteric artery aneurysms. 80% of HAA’s are extrahepatic and 20% intrahepatic. The commonest cause today is probably atherosclerosis. Historically, mycotic aneurysms due to bacterial endocarditis were a common cause, being rare today. Other less common causes include fibromuscular dysplasia, the vasculitides, polyarteritis nodosa and the anastomotic complication of orthoptic liver transplantation.
Physical examination may reveal a pulsatile mass or abdominal bruit, but is usually normal.
Plain film findings may include curvilinear calcification in the right upper quadrant, and a hypoechoic lesion on ultrasound, which may be pulsatile and identified on colour Doppler. Thin collimation contrast enhanced helical CT and contrast enhanced MRI will allow a definitive diagnosis to be made, but the artery of origin may not be clear.
The majority of patients are asymptomatic prior to rupture. Extrahepatic aneurysms may rupture intraperitoneally, and intrahepatic aneurysms may rupture into the biliary tree and cause epigastric pain, haemobilia and obstructive jaundice, called Quincke’s triad. Multiple HAA’s and those of non-atherosclerotic origin are at increased risk of rupture. The risk of rupture related to size is unknown due to the rarity of these aneurysms.
Detailed angiography is required prior to treatment and the latter includes surgical ligation amongst others for extrahepatic aneurysms, with embolization being accepted treatment for intrahepatic aneurysms.
All cases should be considered for treatment, but is has been suggested that HAA’s less than 2 cm in size may be observed, with those 5 cm or more is size definitely being treated.