Post-pancreatectomy Liver Injury After Mayo Clinic Class Ia Celiac Axis Resection: Illustration of This Newly...

Resection of the celiac artery (CA) during surgery for locally advanced pancreatic cancer (LAPC) carries a significant risk of hepatic and gastric ischemia.^1,2 In addition, in the current context, where patients undergo intensive chemotherapy before surgery, a new complication has emerged: post-pancreatectomy liver injury (PPLI).³ PATIENT AND METHODS: A 59-year-old patient with biopsy-confirmed locally advanced pancreatic cancer arising from the pancreatic body (Video and Fig. 1) underwent extended neoadjuvant FOLFIRINOX (folinic acid [leucovorin], fluorouracil, irinotecan, and oxaliplatin). The patient was restaged using the A-B-C criteria,⁴ adding the target approach for anatomical feasibility,⁵ metabolic imaging, and survival prediction.⁶ Fig. 1 Preoperative planning and first operation: extended pancreatosplenectomy, including resection of the left adrenal gland and the celiac artery (CA) (Mayo Clinic class Ia), divestment of the superior mesenteric artery, and portal vein (PV)-superior mesenteric vein reconstruction using a left renal vein graft interposition (A and B). Abdominal phase computed tomography scan, axial view, showing the encasement of the CA but with a free proper hepatic artery (PHA) as a "suitable target" if needed. (C) Drawing of the tumoral involvement with CA encasement and left/anterior side of the superior mesenteric artery (SMA) abutment. PHA, gastroduodenal artery (GDA), and the biliary tract were free of tumor, allowing a Mayo Clinic class Ia CA resection. 15 mm was the distance measured from the tumor to the GDA, and 28 mm was the distance of SMA abutment on the left side. (D) Operative view highlighting the common hepatic artery (CHA) stump, the remnant head of the pancreas (HoP), the venous reconstruction with left renal vein interposition graft, SMA divestment, and the CA stump. IVC, inferior vena cava; LGA, left gastric artery; LGV, left gastric vein; LRV, left renal vein; SA, splenic artery; SMV, superior mesenteric vein PERIOPERATIVE MANAGEMENT: The patient underwent extended pancreatosplenectomy, including resection of the left adrenal gland and the CA (Mayo Clinic class Ia), divestment of the superior mesenteric artery, and portal-superior mesenteric vein reconstruction using a left renal vein graft interposition. Arterial reconstruction was initially deemed unnecessary, as proper hepatic artery flow was maintained-albeit dampened-via the gastroduodenal artery, confirmed by visual inspection and Doppler ultrasound. Postoperatively, the course was notable for a rapid rise in alanine aminotransferase levels without overt clinical or radiological deterioration (Fig. 2). Emergency re-exploration was undertaken with the objective of hepatic arterial revascularization (Fig. 3). We hypothesized that, in the setting of underlying metabolic dysfunction-associated steatotic liver disease, arterial inflow was insufficient to meet the demands of an already vulnerable parenchyma, with increased intrahepatic resistance further compounding ischemic liver injury consistent with clinically relevant (CR)-PPLI. Liver biopsy confirmed acute steatohepatitis and extensive ischemic necrosis. Fig. 2 Postoperative liver enzyme kinetics during the first postoperative week. Alanine aminotransferase (ALT) levels demonstrated a sharp and rapid increase from the day of surgery to postoperative day (POD) 2, leading to re-operation for a supercharged hepatic artery (HA) revascularization. Following revascularization, ALT levels decreased promptly, with complete normalization of liver biochemical parameters by POD 7. AST, aspartate aminotransferase; CAR, celiac artery resection; INR, international normalized ratio POD, postoperative day Fig. 3 Second surgical procedure: final reconstruction and liver biopsy. (A) Drawing of the final reconstruction with a zoom (B) on the arterial bypass between the right renal artery and the common hepatic artery. (C) Liver biopsy showing acute steatohepatitis, with 75% macro- and micro-vesicular steatosis and extensive ischemic necrosis. (D) Zoom on the area of ischemic necrosis, showing infiltration of the liver by neutrophils, lymphocytes, and plasma cells. CA, celiac artery; CHA, common hepatic artery; GDA, gastroduodenal artery; GSV, great saphenous vein; HoP, head of pancreas; IVC, inferior vena cava; LGA, left gastric artery; LGV, left gastric vein; LRV, left renal vein; PHA, proper hepatic artery; PV, portal vein; RRA, right renal artery; RRV, right renal vein; SMA, superior mesenteric artery; SMV, superior mesenteric vein CONCLUSION: Early postoperative recognition and grading of CR-PPLI is critical to prevent liver failure, as static imaging may fail to reflect dynamic hepatic perfusion. A disproportionate rise in alanine aminotransferase within 48 h is a key warning sign. Prospective multicenter studies are needed to better define the incidence, risk factors, and optimal management of CR-PPLI.