Esophageal stents may actually potentiate the TEF-associated pathology. In one report, giant TEFs were induced by esophageal stents placed for a benign stricture or esophageal perforation [17]. The radial force of self-expanding esopha­geal stents has the potential to enlarge the TEF or exclude abscesses that would normally drain back into the esophagus. Another concern is that stenting does not address mediastinal sepsis that may accompany anastomotic disruptions or gas­tric conduit necrosis. Persistent mediastinal con­tamination and inflammation not only leads to TEF, but may also result in aortoesophageal fis­tula, which is almost uniformly fatal. One report, in which a silicone airway stent controlled a PETEF, describes a patient who eventually suc­cumbed to hemorrhage that appeared suspicious for aortogastric fistula [18]. A further concern with airway stenting is that it induces inflamma­tion and granulation. This may extend the length of airway injury, which complicates or precludes definitive operative repair. A technical difficulty with esophageal stent deployment for the PETEF is that there is only a limited esophageal length to accommodate the stent after a cervical anas­tomosis. Additionally, the anastomosis, conduit, and esophagus are relatively capacious relative to the stent’s diameter, and stent migration and poor sealing of the fistula are common.