Restoring the perfusion of accidentally transected right gastroepiploic vessels during gastric conduit harvest for esophagectomy using microvascular anastomosis: a case report and literature review.

BACKGROUND: Esophagectomy remains the standard treatment for esophageal cancer or esophagogastric junction cancer. The stomach, or the gastric conduit, is currently the most commonly used substitute for reconstruction instead of the jejunum or the colon. Preservation of the right gastric and the right gastroepiploic vessels is a vital step to maintain an adequate perfusion of the gastric conduit. Compromise of these vessels, especially the right gastroepiploic artery, might result in ischemia or necrosis of the conduit. Replacement of the gastric conduit with jejunal or colonic interposition is reported when a devastating accident occurs; however, the latter procedure requires a more extensive dissection and multiple anastomosis. CASE PRESENTATION: A 61-year-old male with a lower third esophageal squamous cell carcinoma (cT3N1 M0) who received neoadjuvant chemoradiation with a partial response. He underwent esophagectomy with a gastric conduit reconstruction. However, the right gastroepiploic artery was accidentally transected during harvesting the gastric conduit, and the complication was identified during the pull-up phase. An end-to-end primary anastomosis was performed by the plastic surgeon under microscopy, and perfusion of the conduit was evaluated by the ICG scope, which revealed adequate vascularization of the whole conduit. We continued the reconstruction with the revascularized gastric conduit according to the perfusion test result. Although the patient developed minor postoperative leakage of the esophagogastrostomy, it was controlled with conservative drainage and antibiotic administration. Computed tomography also demonstrated fully enhanced gastric conduit. The patient resumed oral intake smoothly later without complications and was discharged at postoperative day 43. CONCLUSION: Although the incidence of vascular compromise during harvesting of the gastric conduit is rare, the risk of conduit ischemia is worrisome whenever it happens. Regarding to our presented case, with the prompt identification of the injury, expertized vascular reconstruction, and a practical intraoperative evaluation of the perfusion, a restored gastric conduit could be applied for reconstruction instead of converting to more complicated procedures.

Disrupted hepatic adiponectin signaling impairs liver regeneration of steatotic rats.

BACKGROUND: Individuals with non-alcohol fatty liver disease (NAFLD) exhibit impaired liver regeneration in a clinical setting and animal experiments. Adiponectin signaling is recognized as an important pathway of lipid metabolism, energy expenditure, anti-inflammation, and cellular proliferation. We herein investigate hepatic adiponectin signaling in dietary steatotic murine models undergoing hepatectomy, which has never been explored. METHODS: Sprague-Dawley rats fed with a normal diet (normal), high fat diet (HF), and a methionine-choline deficiency diet for 1 week (MCD 1W) and 5 weeks (MCD 5W), were used. The animals underwent 70% hepatectomy and were thereafter sacrificed at indicated time points. RESULTS: MCD 5W and HF displayed decreased Ki-67 labeling index and restituted liver mass compared to normal. Hepatic adiponectin, as well as TNF-α, of MCD5W and HF were increased compared to normal; whereas adiponectin receptor type 1 (AdipoR1) and adiponectin receptor type 2 (AdpoR2) were reciprocally decreased when compared to normal. PPARα, a downstream molecule of AdipoR2 axis, was decreased in MCD 5W compared to normal. Adenosine monophosphate- activated protein kinase (AMPK), a downstream molecule of AdipoR1 axis, was inactivated soon after hepatectomy in normal; whereas activation of AMPK persisted until day 3 after hepatectomy in MCD 5W and HF. CONCLUSIONS: Reciprocal expression of adiponectin and its receptors in steatotic rats represents a unique form of adiponectin signaling disruption, which might be associated with impaired liver regeneration.