Gastric tube necrosis (GN) following esophagectomy is a rare, but critical and life threatening complication. Unlike anastomotic leakage due to local ischemia, GN involves extensive full thickness ischemia resulting from… Click to show full abstract
Gastric tube necrosis (GN) following esophagectomy is a rare, but critical and life threatening complication. Unlike anastomotic leakage due to local ischemia, GN involves extensive full thickness ischemia resulting from vascular insufficiency. Most cases of GN need total or partial replacement of gastric tube. Although quantitative assessment of tissue perfusion during esophageal surgery contributed to reduce the incidence of postoperative anastomotic complications, GN remains a serious complication to be solved. Data were collected retrospectively from 271 patients who underwent esophagectomy and gastric tube reconstruction at a single center between 2008 and 2018, in which cases of GN were identified. Gastric mobilization was mainly performed laparoscopically using a hand-assisted maneuver. The short gastric and left gastric arteries were divided, and the right gastric and gastroepiploic arteries were both preserved. The gastric tube 3.5 cm in width was created along the greater curvature. Intraoperative assessment of perfusion of the gastric tube was performed using our novel Thermal Imaging System (TIS) in all patients. Quantitative tissue perfusion scores defined as anastomotic viability index (AVI) were calculated at various points from the anastomosis. The inpatient mortality rate was 1.8% (n = 5). Anastomotic leak (AL) developed in 8.8% (n = 24) of the study group. The mean AVI score of cases with AL was 0.58, which was significantly lower than that without AL (0.71, P < 0.001). GN occurred in two patients (0.7%). The AVI score of the both GN cases were relatively high at 0.74 and 0.82. In one of the cases, circumferential full thickness ischemia 10 cm in length from the esophagogastric anastomosis was revealed by contrast CT scans and endoscopy, which was later identified to be due to severe vascular impairment. TIS can be used as a reliable intraoperative assessment tool for perfusion of the gastric tube. We assume that most AL would be caused by delayed anastomotic healing due to poor vascularization of the gastric tube. On the other hand, obvious difference in AVI scores between AL and GN may indicate the involvement of different etiology. Given that development of GN seemed to be caused by acute failure in vascularization during the early postoperative period. All authors have declared no conflicts of interest.
               
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