Authors’ reply

our endoscopic armament for direct lesional hemostasis, through its tamponade effect and vasoconstriction, precisely what one would want to avoid in ischemic organ injury. The risk of perforation is also highest in the esophagus, which notably lacks serosa, an additional layer of protection common to the rest of the gastrointestinal tract. It is for this reason that epinephrine injection should be avoided and, importantly, stent placement should not be performed. Indeed, there have been reports of perforated BE in the setting of stent use [5]. Finally, in asymptomatic patients, repeat endoscopy may be helpful in verifying the normalization of the mucosal lining and excluding occult pathology that could have been masked by diffuse BE on initial presentation. This may be performed a few weeks past therapy and should not delay the patient’s discharge from the hospital once stable. Stricture or stenosis formation in AEN, which occurs in over 10% of cases during Stage 2 and 3 of the disease, may have an association with concurrent duodenal pathology [2] and seems to be inversely related to the state of immune compromise in affected patients with diabetes mellitus, malnutrition and malignancy [6]. Stricture or stenosis could be managed with outpatient endoscopic dilatation and antacid therapy, but repeat sessions may be necessary. In the past decade, AEN has continued to ascend the differential diagnosis ladder in hospitalized patients presenting with upper gastrointestinal hemorrhage, largely because of the increased use of endoscopic procedures. Its prompt recognition and proper management will remain important for decreasing mortality and improving the patient’s outcome.