Within the field of interventional radiology, there has been a recent explosion of interest in trans-arterial therapies related to the liver and foregut organs including chemo- or radio-therapy, and various embolization techniques. The continual development of such interventions highlights the importance of understanding the variability in hepatic arterial anatomy.
This patient had a proper hepatic artery (with both right and left hepatic branches) arising from the expected location in the celiac axis. Thus, the artery arising from the SMA and giving off multiple branches to supply the duodenum could only be a replaced GDA. This vessel continued as an accessory LHA, likely supplying segments II and III. To the authors’ knowledge, this anatomic variation of the GDA with an accessory LHA is not described elsewhere.
The traditional classification of anatomic variation of the hepatic artery was introduced by Michels in 1955, where much of the known anatomic variability was identified by cadaveric dissection (Michels 1955). More recent meta-analyses and large surgical and radiological studies have offered a range of classification systems for the celiac trunk and CHA, and a review of this literature confirms how unique this variant may be (Noussios et al. 2017; Panagouli and Venieratos 2013; Hiatt et al. 1994; Song et al. 2010).
Panagouli et al. published a meta-analysis of celiac axis variation including 12,000 cases from 36 studies, and described a CHA replaced to the SMA in 1.13% of cases (Panagouli and Venieratos 2013). There was, however, no description of GDA replacement in the setting of a normal proper hepatic artery (PHA) from celiac trifurcation. Hiatt et al. described variant hepatic anatomy in 1000 patients who underwent hepatectomy, with a similar 1.5% rate of CHA replacement to the SMA, but again without mention of a PHA from the celiac axis (Hiatt et al. 1994). Likewise, Covey et al. described hepatic arterial anatomy in 600 patients evaluated by DSA, with 12 (2%) patients having CHA replaced to SMA, and 2 (0.3%) patients having PHA replaced to SMA with GDA coming directly from the aorta (Covey et al. 2002).
Most notably, Song et al. described 5002 patients by CT or DSA and described a replaced GDA in 1.1% of patients (specifically replaced to the SMA in 0.8% of patients), however there was no description of the GDA continuing into a hepatic arterial component (Song et al. 2010). Not surprisingly, this variant of an accessory LHA arising from the replaced GDA, with proper right and left hepatic arteries arising from a PHA is not readily explained by the anatomic model put forth by Song et al. They proposed a multi-level precursor anastomotic arterial pathway, part of which involves a primitive anastomosis of the left gastric artery, left hepatic artery, and celiac axis (the so-called “Lesser omental pathway”). This pathway would thereby explain the commonly-seen replacement of the LHA to the left gastric artery. This model, however, does not explain an accessory LHA arising from a replaced GDA.
An entirely replaced LHA on a GDA replaced to the SMA is described in 1 case report by Younan et al., however the patient described here is of added interest due to the incongruity with the previously published anatomical model described above (Younan et al. 2016). An entire LHA arising from the GDA conforms with Song’s anatomical model. In contrast, their “lesser omental pathway” does not communicate with the GDA and thus a new anastomotic channel would have to be conceived to explain the variant described here as this patient’s proper LHA maintains its normal anatomical location.
From a procedural perspective, this case demonstrates the importance of thorough interrogation of both the celiac and SMA axes during mesenteric angiogram. Upon initial nonvisualization of a GDA on celiac angiography, it may have been assumed that the GDA was in spasm or constricted secondary to epinephrine injection. However, secondary SMA angiography was critical in revealing the bleeding replaced GDA.
Upon discovery of this anatomic variant with terminal supply in the liver, it was considered intraoperatively that embolization of the GDA might result in ischemia of the downstream left lateral section of the liver. However, the patient had already received 6 units of packed red blood cells between the emergency department and the GI lab, and in the emergent setting presented here, and without known hepatic disease, this partial hepatic ischemia was determined to be an acceptable risk. Not surprisingly, this patient developed a mild transaminitis (AST = 107 u/L) on post operative day 2, which resolved 2 weeks later. The subsequent liver injury further corroborates the aberrant hepatic supply described above.
Interventional radiologists must have a comprehensive understanding of not only the standard hepatic and foregut arterial anatomy but also its variants in order to avoid complications, treatment failure, excessive radiation and contrast administration. The anatomical variant described here would have implications for interventional oncology in particular, where a treatment dose may need to be split during radiation lobectomy. Additionally, variations of hepatic arterial anatomy such as this are of particular importance for hepatobiliary surgeons. For example, variant arterial supply can complicate vascular dissection in organ procurement/transplantation or curative resection in surgical oncology (Younan et al. 2016).
