54.2% of AEF are due to aneurysm rupture initiated by arteriosclerotic, syphilitic, or traumatic mechanisms (3). Ingestion of foreign bodies (bones from animal foods, sharp metal objects) is the next common cause of aortic-esophageal fistulas at 19.2%. This is followed by esophageal malignancy (17.0%) and post-surgical fistula formation. Consequently, the yearly incidence is approximately one case associated with esophageal cancer. Chiari first describes the aortoesophageal fistula syndrome, as a painful radiation to the back, followed by a “signal hemorrhage”, then a lucid interval Inhibitors,research,lifescience,medical (asymptomatic period) (4), (5). Soon afterwards, overt exsanguinations

can occur within hours to days later. One review states that 65% of AEF patients have sentinel bleed reported, and 59% of patients recall a history of chest pain (2). However, very few AEF patients with an underlying esophageal malignancy present with all symptoms of the Chiari syndrome (2). Our patient had sentinel hemorrhage without mid-thoracic Inhibitors,research,lifescience,medical pain, followed by immediate exsanguination after a short lucid interval of few minutes in the

ICU. As for Inhibitors,research,lifescience,medical the formation of AEF, Postoloff et al. along with other observers support that aortic perforation is caused by thrombosis of the vaso vasorum, accelerating the fistula formation between aorta and esophagus (5)-(7). However, Postoloff reports three additional theories on esophageal perforation into the aorta (8): i) invasion with most reported tumors seen only in the adventitia (2); ii) bacterial infection (9); iii) ulcerative process as tumor disintegrates (10). On autopsy, our patient’s esophagus shows a deep ulceration

Inhibitors,research,lifescience,medical with extensive necrosis and fibrosis involving the entire thickness of the esophageal wall, extending into the media of aorta. The ulcerative lesion of esophagus is measured to be 3.5 x 2.5 x 0.5 cm with a fistula tract between esophageal lesion and superior part of descending aorta, as seen grossly on the esophageal and aortic views in Figure 2A and Inhibitors,research,lifescience,medical 2B, respectively. Scattered atypical large cells, focally clustered, are seen within the area of necrosis, consistent with residual squamous cell carcinoma altered by chemo-radiation (Fig. 3A). On section Navitoclax cell line immunoassays, these cells are positive for cytokeratin AE1/AE3 and are negative for both synaptophysin ARN-509 and neurofilament protein (Fig. 3B). However, no evidence of thrombosis in the vaso vasorum is observed, and other pathologic studies report similar findings (2), (6), (8). Figure 3 A) There are scattered atypical large cells, focally clustered, within the area of necrosis, consistent with residual squamous cell carcinoma with marked radiation changes. B) On section immunoassays, these cells are positive for cytokeratin AE1/3 and … In this case, the formation of AEF is not through the thrombosis of vaso vasorum, but by the tumor’s ulcerative and infiltrative process.