|Home | About | Journals | Submit | Contact Us | Français|
The present report describes a case of an extrahepatic right hepatic artery pseudoaneurysm caused by acalculous cholecystitis. An 85-year-old man was admitted with abdominal pain, cachexia and jaundice. A CT scan showed a saccular false right hepatic artery aneurysm within a soft tissue and fluid mass that was causing biliary obstruction. The soft tissue mass raised the possibility of malignant disease, but this resolved slowly after a period of time and on reviewing the patient's history the only upper gastrointestinal problem noted was an episode of acalculous cholecystitis 3 months previously, which was believed to be the cause of the pseudoaneurysm. The false aneurysm was treated successfully with coil embolisation and the patient recovered fully from this illness.
Right hepatic artery pseudoaneurysm is rare and has not been described following acalculous cholecystitis. Our patient had a mild episode of acalculous cholecystitis and was treated in hospital with antibiotics for only 3 days 3 months previously. There were no gallstones on ultrasound and there had been no evidence of pancreatitis, which would be a condition more likely to cause pseudoaneurysm formation. As a soft tissue mass was found on CT, the other consideration was whether there was a malignant process causing the pseudoaneurysm, which would also be a more likely cause of pseudoaneurysm formation. Our patient had significant biliary obstruction and haemobilia, which were difficult to treat with endoscopic retrograde cholangiopancreatography (ERCP) due to access issues, and in an 85-year-old patient this could have been thought to be a terminal event due to the likelihood of malignancy; however, this case demonstrates that seemingly benign conditions can potentially mimic malignant processes and have a good outcome when treated.
An 85-year-old man was seen as an outpatient, having been referred via the 2-week wait system with intermittent epigastric pain, constipation, mild normocytic anaemia and deranged liver function tests (LFTs). The patient had been previously admitted with epigastric pain and ultrasound had shown a thick-walled gallbladder and no stones, and a diagnosis of acalculous cholecystitis had been made. An urgent outpatient CT was requested but the patient was admitted before this was performed with abdominal pain, cachexia and jaundice.
On admission the patient had mild right upper quadrant tenderness with a palpable liver edge. His blood results showed evidence of sepsis (white cell count 13.1 x 109/l, C reactive protein 91 mg/l) and his liver function was now profoundly deranged (bilirubin 230 micromols/l, alanine transaminase 145 IU/l, alkaline phosphatase (ALP) 927 IU/l, albumin 33 g/l and international normalised ratio of 1.3).
A CT scan was performed that showed an inflammatory mass of abnormal soft tissue and fluid around the gallbladder, compressing his common bile duct causing gross intrahepatic duct dilatation. Within this mass was a 19×8×8 mm saccular false aneurysm arising from the right hepatic artery. Blood cultures grew Staphylococcus, which was thought to be a skin contaminant.
The differential diagnosis of the soft tissue mass surrounding the pseudoaneurysm was inflammation secondary to acalculous cholecyctitis or pancreatitis or malignancy, most likely carcinoma of the pancreas.
The patient was given oral ciprofloxacin on admission. Management was initially via ERCP and stenting to try to decompress his bile duct prior to more definitive management of his hepatic artery aneurysm. However, the patient had persistent haematobilia that caused clots to continue to obstruct his biliary tree, although the blood loss was not at any point profound enough for him to become unstable. In view of this the patient underwent embolisation of his right hepatic artery, which arose from the superior mesenteric artery. The aneurysm could not be excluded with use of a stent graft due to the complexity of the anatomy requiring navigation. In addition, at the time of the procedure the aneurysm had enlarged in size considerably from the time the CT was performed (figures 1–4) and there was no suitably large stent available.
After embolisation his jaundice improved (despite a slight initial rise in alkaline phosphatase thought to be secondary to a mild degree of ischaemic hepatitis), and the patient was discharged home after a period of rehabilitation. A repeat CT scan showed no filling of the aneurysm and occlusion of the right hepatic artery with normal liver parenchyma. The inflammatory phlegmon had almost resolved although there was still a degree of intrahepatic duct dilatation and his jaundice did not fully resolve. The patient was well and putting on weight at 3-month follow-up.
Right hepatic artery aneurysm is uncommon. The incidence of all visceral artery aneurysms is thought to be 1%, with hepatic artery aneurysm forming approximately 20% of this group.1–3 A recent review of experience with visceral artery aneurysms in 1 centre over 25 years yielded 55 cases, of which 7 were common hepatic and none were right hepatic.4 Estimates of incidence are difficult to ascertain on review of the literature, as due to the infrequency of the occurrence each series reporting on visceral artery aneurysms contained different types of aneurysm, including splenic, mesenteric, common hepatic and left hepatic. In addition they can be subdivided into true or false and intrahepatic or extrahepatic, and the pathogenesis is not well known. Various different aetiologies have also been described. Atherosclerosis is thought to be a secondary event1 and the causes reported in the literature include trauma, which is often iatrogenic following surgical or percutaneous hepatobiliary procedures, congenital disorders, immunosuppression and neoplasia, inflammatory disorders such as pancreatitis and infection.5–9 A further problem with the estimation of incidence is that many hepatic artery aneurysms are asymptomatic and incidence may appear to be increasing due to the increased frequency of CT scanning, particularly following blunt abdominal trauma.9
Mycotic aneurysms were more common previously, often secondary to infective endocarditis,10 however, with changing patterns of disease and the increase in surgical procedures, particularly laparoscopic cholecystectomy and percutaneous liver biopsy, iatrogenic injury to the artery is now the most common cause and in many series mycotic aneurysms are rare.11 12 Infections cited in the literature include embolic phenomenon from infective endocarditis, which is now mainly seen among intravenous drug taking populations, severe systemic sepsis and amoebic infections.13 In addition immunosuppression has been reported as a cause for mycotic aneurysms in conjunction with liver transplantation or treatment for other malignancies or disorders such as Crohn's disease.14–16 This case is particularly interesting as it occurred in a case of presumed acalculous cholecystitis that was not severe as it necessitated only a short admission and no intervention other than antibiotic treatment at that time.
This case also highlights some of the diagnostic difficulty that can occur with hepatopancreatobiliary lesions. The differential diagnosis of the mass abutting the common bile duct in an 85-year-old man with cachexia is carcinoma of the head of the pancreas, particularly as neoplasia is a better known cause of right hepatic artery false aneurysm than acalculous cholecystitis. No biopsies were possible due to anatomical position and those taken at ERCP were normal. This could have caused management and decision-making difficulties in the case of massive haemobilia with resulting instability.
On review of the literature, although embolisation of the aneurysmal artery is now well recognised as preferred management of these lesions, it is worth noting that our patient is one of the oldest on record to undergo this procedure.1 2 5 9 16 As stated above, a stent graft to maintain patency of the vessel while excluding the aneurysm was not possible. Embolising the artery causes a degree of right hepatic lobe ischaemia, which we believe was the cause of our patient's persistently deranged, albeit improved LFTs (bilirubin 99, ALP 271). Despite this degree of physiological insult and his general frailty the patient did well clinically and put on some weight.
In summary, this case is a worthy addition to the literature as it highlights that a supposedly benign case of acalculous cholecystitis can cause right hepatic artery false aneurysm, and this responds well to treatment with embolisation in an older patient.
We thank to the patient, as the patient had a keen interest in medical science, and to the patient's family who consented after his death.
Competing interests None.
Patient consent Obtained.