The prevalence of hepatic artery (HA) aneurysms is low, and they are mainly caused by atherosclerosis (30-35%)¹. Other less common etiologies include infections (mycotic aneurysms), lupus or polyarteritis nodosa¹. Hepatic artery aneurysms account for 20% of all visceral aneurysms and 80% are extrahepatic^1,2.

They are usually asymptomatic and present as an incidental finding^1-3. Expanding aneurysms should be suspected in case of abdominal pain and vagal reaction; other presentations include signs and symptoms of cholestasis and gastrointestinal bleeding (if an arterial fistula is present)^2,3.

Surgical or endovascular treatment is indicated in symptomatic aneurysms or those > 25 mm due to their high risk of rupture¹. There are no significant differences between surgery and endovascular procedures in terms of mortality, but endovascular treatment is preferred in patients with comorbidities³. A 69-year-old male patient sought medical care due to sudden and intense epigastric pain associated with profuse sweating. He had a history of hypertension, diabetes and was receiving anticoagulants due to chronic atrial fibrillation and immunosuppressants (prednisone and everolimus) due to a kidney transplantation in 1993. On physical examination the patient was hemodynamically stable and presented generalized jaundice. The abdomen was tender on palpation without rebound tenderness.

There were no signs of pneumoperitoneum on plain abdominal X-ray. Laboratory tests showed a cholestatic pattern; total bilirubin (TB) of 3.1 mg/dL with direct bilirubin predominance, alkaline phosphatase of 400 U/L, gamma-glutamyl transpeptidase of 630 U/L, aspartate aminotransferase (ASAT) of 220 U/L and alanine aminotransferase (ALAT) of 320 U/L.

On abdominal ultrasound, the bile duct was dilated; the common bile duct had a diameter of 15 mm and there was a hypoechoic solid nodule of 45 mm in the head of the pancreas. In view of this finding, a computed tomography (CT) scan was ordered. The common hepatic artery (CHA) had a fusiform dilatation consistent with an aneurysm with calcified walls, and another aneurysm dilatation was observed in the origin of the gastroduodenal artery (GDA) with an eccentric thrombus inside that totally occluded the artery lumen. This area caused compression of the distal common bile duct and the spleno-portal axis, which was patent (Fig. 1A).

Figure 1 A: CT scan on admission. B: CT scan in the axial plane obtained during the arterial phase 12 hours after admission, with abnormal shape and density of the tissues adjacent to the aneurysmal dilatations. Hemoperitoneum (black arrow) as sign of aneurysm rupture. C: Coronal maximum intensity projection reconstruction from CT scan in the arterial phase showing aneurysm of the CHA (black arrow), aneurysm of the GDA (black arrowhead) and tortuous fusiform dilation of the PHA (white arrow). D: Coronal maximum intensity projection reconstruction from CT scan in the arterial phase. A right HA emerging from the SMA is identified as anatomical variant (black arrow). 

Twelve hours after admission, the patient experienced recurrent abdominal pain associated with signs of hypovolemic shock; intensive resuscitation with intravenous fluids and vasoactive agents was started, resulting in temporary hemodynamic stability. As the initial diagnostic CT scan was performed in portal phase, the vascular anatomy of the hepatic artery could not be clearly defined. Therefore, a CT angiography was performed, which showed moderate hemoperitoneum around the liver and spleen and changes in the tissue adjacent to the aneurysm, with absence of contrast leakage (Fig. 1B). The presence of an aneurysm was confirmed, involving the distal segment of the CHA, the origin of the GDA and the proximal segment of the proper hepatic artery (PHA) (Fig. 1C). An intimal flap was observed in the CHA as a sign of local dissection of the aneurysm, extending up to the origin of the GDA. Interestingly, the right HA emerged from the superior mesenteric artery (SMA) (Fig. 1D).

Considering the clinical findings and the results of the imaging tests suggestive of ruptured aneurysm of the CHA, an emergency laparotomy was decided due to the hemodynamic status of the patient and the impossibility of performing an immediate endovascular treatment. During the surgical exploration we detected hemoperitoneum of approximately 1500 cm³. A 5- mm aneurysm with minimal wall disruption was identified, macroscopically consistent with a true aneurysm. The aneurysm included the origin of the CHA in the celiac trunk, was 10-mm long and involved the origin of the PHA and the GDA; both arteries also presented aneurysmal dilatation.

The initial indication was placement of a stent graft, from the origin of the CHA to the intact PHA. The aneurysm was then opened. There was an extensive proximal intimal dissection with a false lumen and absence of retrograde flow of the PHA and GDA, which had a thrombus inside (Fig. 2).

Figure 2 A and B: Intraoperative pictures. Left: aneurysm of the CHA involving the PHA and GDA (black arrow). Middle: aneurysm sac opened, with extensive intimal dissection and false lumen (white arrow). C: The image on the right illustrates the intraoperative anatomical situation with the aneurysm of the CHA (black arrow) and the right HA (long black arrow). 

In view of these elements, together with the presence of a right HA originating from the SMA in a hemodynamically unstable patient with a poor anesthetic and surgical setting, the aneurysm was resected and the HA and GDA were ligated in their origin. There were no changes in the color of the liver surface suggestive of hepatic ischemia. In the postoperative period the patient initially developed acute hepatitis with a cholestatic pattern which was interpreted as secondary to ischemia, with elevated ALAT and ASAT levels (1800 and 2000 U/L, respectively) and TB levels of 8.04 during the first 72 hours, which decreased thereafter. The patient remained in the intensive care unit (ICU) for 7 days and was discharged 14 days later, due to favorable progress. As the incidence of HA aneurysms is low (0.002-0.4%)^2,3, there are few studies on this condition which have been carried out on case series by collecting isolated experiences and analyzing the experience gained. Therefore, the scientific evidence for its management is scarce.

Between 40% and 60% are asymptomatic in case of rupture, with an overall mortality of 35- 70%^1,2. For this reason, early diagnosis and treatment is important. Imaging tests as CT scan or CT angiography, or both, play an important role in the early detection of complications and mainly for planning the surgical approach⁴. Deciding between endovascular and surgical approaches depends on several factors: clinical presentation, site and extent of the aneurysm, patient’s status and the experience of the treating team⁴. Yet conventional surgery is usually the option in emergency interventions.

The aim of surgery is to exclude the aneurysm sac from the systemic circulation, ideally preserving the distal blood flow by placing an autologous graft or synthetic graft⁵. This is mandatory when the aneurysm involves the PHA^2,5,6. Bypass is justified since the PHA provides almost 50% of the oxygenated blood to the liver, and its ligation as a terminal artery may cause ischemia and liver failure^5,6. However, when the aneurysm involves only the CHA and the root of the gastroduodenal artery is normal or the right HA originates from the SMA, a bypass is unnecessary. For this reason, it is essential to determine the location and extent of the aneurysm, the status of the collateral hepatic circulation, and any possible anatomical arterial variants to determine the best treatment^4-7. The modified Michels classification⁸ describes the anatomical variations of the hepatic artery. If we consider the concept of preserving the terminal blood flow to the liver, mainly to the right liver, there are two types (type 1 and 2) in which bypass is mandatory, which are present in 70% of the population. For the remaining group, liver revascularization would not be necessary after excluding the aneurysm sac, thus facilitating the surgical procedure and significantly reducing operative times.

For this reason, an exhaustive preoperative search should be carried out to detect accessory hepatic arterial variants mainly in the area between the inferior vena cava and the dorsal surface of the duodenal-pancreatic block for the detection of a right HA, and in the Arantius’ ligament for a left HA. This case illustrates how a bypass graft can be avoided in the presence of “non-conventional” hepatic arterial anatomy, which occurs in approximately one third of the cases, facilitating the operative procedure and resulting in a significant impact on morbidity and mortality.