The aim of this study was to report the incidence, risk factors, and management of gastric conduit dysfunction after esophagectomy in 177 patients over a 3-year period in a single center. Patients with anastomotic strictures or delayed gastric emptying (DGE) were identified from a prospective database. Anastomotic strictures occurred in 48 patients (27%). Eighty-three percent of early anastomotic strictures (<1 year) were benign, and all late strictures (>1 year) were malignant. Dilatation was effective in 98% of benign and 64% of malignant strictures. DGE occurred in 21 patients (12%), and was associated with both anastomotic leak (P = 0.001) and anastomotic stricture (P = 0.001). 4/8 patients with late DGE (>3 months postesophagectomy) were tumor-related. Pyloric dilatation was effective in 92% of early and 63% of late DGE. Pyloric stents were inserted in 3 patients with tumor-related DGE. After esophagectomy, early anastomotic strictures (within 1 year) and early delayed gastric emptying (within 3 months) are usually benign and respond to dilatation. However, patients presenting later with tumor-related obstruction are unlikely to respond to anastomotic or pyloric dilatation and should be stented.

Introduction Gastric tube necrosis following oesophagectomy is thought to have an increased association with a minimally invasive technique. Some suggest gastric ischaemic preconditioning may reduce ischaemic complications. We discuss our series of 155 consecutive minimally invasive oesophagectomies (MIOs), including a number of cases of gastric tube ischaemia, of which 4 (2.6%) developed conduit necrosis. Methods Data were collected prospectively of MIOs carried out by a single surgeon between 2005 and 2011. Cases of gastric tube necrosis were identified. Results Overall, 155 patients were identified. The inpatient mortality rate was 2.6%. Gastric tube necrosis occurred in four patients (2.6%). An ultrasonic dissector injury to the gastroepiploic arcade had occurred in two cases. In another case, the gastric tube was strangulated in the hiatus. In the remaining case, no clear mechanical cause was identified. All 4 cases occurred within the first 73 cases. The gastric tube necrosis rate of the first 50 cases versus cases 51–155 was 4% and 2% respectively (p=0.5948). The anastomotic leak rate in these two cohorts was 18% and 7% respectively (p=0.0457). There was a significant reduction in overall gastric tube complications from 22% to 10% following the learning curve of the initial 50 cases (p=0.0447). Conclusions In our series, gastric tube necrosis appears to be a learning curve issue. Prophylactic measures such as ischaemic preconditioning become less relevant as the operating surgeon’s experience increases. Instead, meticulous attention to preserving the gastroepiploic arcade, avoidance of tension in the tube and careful positioning of the gastric conduit through an adequately sized hiatus are key factors.

The antireflux stent had no demonstrable advantages compared to the combination of standard open stent and proton pump inhibitor medication.