Effectiveness of fibrin sealant as a hemostatic technique in accelerating endoscopic submucosal dissection-induced ulcer healing and preventing stricture in the esophagus: A retrospective study

Abstract

The aim of the present retrospective study was to evaluate the effectiveness of conservative electrocoagulation followed by porcine fibrin sealant (FS) as a protective hemostatic technique for wounded microvessels in promoting the healing of endoscopic submucosal dissection (ESD)-induced ulcer, and preventing esophageal strictures that follow ESD. A total of 203 patients with early esophageal cancer or precancerous lesions were retrospectively analyzed. The 1-month ulcer healing and stricture rates were compared between the two groups (combined hemostats and electrocautery groups). The 1-month complete healing rate was 77.0% in the combined hemostats group and 52.6% in the electrocautery group (P=0.003). The use of FS and a smaller resected range (<3/4 circumference) was associated with a better 1-month healing rate. For patients with a ≥3/4 circumference mucosal defect, the esophageal stricture rate was 31.6% (6/19) in the combined hemostats group and 25.0% (2/8) in the electrocautery group. There was no difference in the stricture rate (P=0.737) and dilation time (P=0.733) between the two groups. In conclusion, the application of conservative electrocoagulation followed by porcine FS as a wound-protection technique promoted ESD-induced ulcer healing in the esophagus. However, this combined hemostatic technique was not superior to the conventional hemostatic method in preventing post-ESD stricture in patients with large esophageal mucosal defects.

Feasibility of same-day discharge following endoscopic submucosal dissection for esophageal or gastric early cancer

“…We did not perform prophylactic coagulation on nonbleeding visible vessels smaller than 0.3 mm in the post-ESD ulcer. Our previous study showed that a wound microvessel-protective hemostatic technique followed by porcine fibrin sealant can promote ESD-induced ulcer healing without increasing delayed bleeding events[ 15 ]. Prophylactic hemostasis-induced tissue damage or necrosis may lead to the exposure of arteries on the base of the ulcer, which in turn would contribute to delayed episodes of bleeding[ 21 ].…”