Letter to the Editor: Aberrant arteries—1 may be better than 2 for the liver, but maybe not the bile duct

Dear Editor, We read the recent publication by Pravisani and colleagues and its associated editorial article with great interest.1,2 This study describes a practical approach to the management of aberrant left (aLHA) and right (aRHA) hepatic arteries. Such a study is only possible in a highly organized unit whereby all surgeons adopt the agreed approach. In our practice, we also perform selective reconstruction of aLHA, but the decision is based on vessel size in a manner similar to that described by Montalti et al.3 This is based on the premise that thrombosis of a small aberrant left may propagate retrograde into the main artery, hence may prove to be counterproductive in the long run. Furthermore, ligation of a small aLHA that originates from the left gastric (by far the most common) 4 allows the main anastomosis to be as distal as possible to avoid redundancy and the tendency for vessel kinking. However, herein lies our first problem with the approach outlined by Pravisani and colleagues. Once reconstruction at the gastroduodenal artery level is performed, and if intraoperative ultrasound suggests a low resistive index, aberrant vessel reconstruction would need to be through a vessel other than the native hepatic artery. Although not impossible, this would present a higher technical challenge and risk than conventional reconstruction. A “One artery” approach maybe sufficient for the liver parenchyma, but we would argue that it is insufficient for the extrahepatic bile duct and suggest the results by Pravisani and colleagues reflect this issue. An aRHA courses along the posterolateral aspect of the extrahepatic bile duct up to the liver. This vessel supplies not only the liver but also the common bile duct, as demonstrated in corrosion cast studies.5 Intraoperative ultrasound of the liver parenchyma, being advocated by Pravisani and colleagues, may not detect the lack of arterial microcirculation in the peribiliary plexus. This is thought to result in anastomotic strictures in both liver transplantation and wider hepatobiliary surgery. The subgroup analysis by Pravisani and colleagues showed a rate of early biliary strictures to be 7/40 (17.5%) in the ligated aRHA group, as opposed to 47/499 (9.5%) (p = 0.166). This could reflect a type 1 error due to the small sample size of the ligated group. A comparison between the reconstructed aRHA with the ligated aRHA subgroup maybe more useful; however, this will also be troubled by small numbers. Nevertheless, this represents an important study that challenges some of our long-held beliefs, and the authors should be commended.