Objectives. Upper digestive hemorrhage from acute esophageal postbanding ulcers is a rare complication of endoscopic banding, but with high morbidity and mortality. The incidence of this event reported in the literature varies widely between 2.3% and 18%. Risk factors are not well studied. They may be caused by reflux of gastric acid into the lower esophagus, leading to exposure of ulcer(s) and underlying vein(s) to the acid. Alternate explanations include slippage of bands, infection of ulcers, and coagulopathy that leads to increased bleeding. Remarkably, there is no clinical or endoscopic classification based on the morphology of these lesions (ulcers), or which associates endoscopic appearance with clinical outcomes. Therapeutic management recommendations are absent or sporadic. So, the given objectives include a study of the available literature and data analyses pointed to the etiology, pathogenesis, practical classification and endoscopic treatment of the acute esophageal postbanding ulcers. Materials and methods. A structured search was performed in the electronic database, taking into account relevant articles, published in the last 10 years. The profile literature has been studied on “PubMed”, “NCBI”, “HINARI”, “Cochrane Library” platforms. Advanced search mod was applied, using keywords in english („postbanding upper digestive hemorrhage”, „endoscopic bandage”, „esophageal stenting”, ”postbanding ulcers”, „severe liver disease”). Results. Several ways of endoscopic treatment were highlighted such as: filling with adhesive tissue (cyanoacrylate) or fibrin complex, injection of sclerosing agents (aethoxisclerol), rebanding, mounting the Sengstaken-Blakemore tube, heamospray usage, endoclips application (simple ones or OVESCO type), Danis type stent insertion. No systematic reviews or meta-analyses were found on this topic. The appropriate postbanding ulcers classification seems to be the Jamwal-Sarin system, based on their endoscopic appearance in descending order as types A, B, C and D. Each type included ulcers with or without bands in situ. In type A, there was active spurting from the ulcer. Type B was characterized as active oozing from the ulcer. In type C, the ulcer appeared with a pigmented base or a visible clot. The type D ulcer had a clean base (white or yellow). Conclusions. The minimally invasive conduit of acute postbanding ulcer bleeding is controversial and not well established. Further studies are required to standardize the endoscopic approach to this complication. Stratifying patients based on Jamwal-Sarin type can help predict outcomes, independent of the non-endoscopic (MELD, Child) scoring systems. Classifying acute postbanding ulcers by endoscopic morphology may direct treatment strategies, and warrants further validation.