Delayed esophageal perforation secondary to thoracic aortic replacement or thoracic endovascular aortic repair (TEVAR) is a rare but potentially fatal condition [2, 4,5,6,7].
Seto et al. reported that although the exact mechanism of secondary esophageal perforation after stent grafting remains unknown, hypotheses include (1) direct erosion of the stent graft into the esophagus, (2) pressure necrosis caused by the self-expanding endoprosthesis, (3) ischemic esophageal necrosis due to disruption of the arteries that feed the esophagus, (4) infection of the stent-graft prosthesis (artificial graft for aortic replacement was included in our case), (5) pseudoaneurysm development, and (6) endoleakage into the residual aneurysmal sac .
In our cases that was performed aortic replacement procedure (nos. 1–6), (3) and (4) were thought to be a possible cause. In addition, no. 3 case had potential for (2), and no. 5 had potential for (2) and (5). No. 7 with Marfan syndrome had highly potential for (5) and (6). There was no equivalent case for (1).
We consider the hypothesis that ischemic esophageal necrosis due to disruption of the arteries that feed the esophagus should be focused. The thoracic esophagus is fed by bronchial and esophageal branches of the thoracic aorta. Aortic replacement or stent grafting can potentially damage these feeding arteries of the thoracic esophagus. We consider that the relatively long period from cardiovascular surgery to esophageal perforation supports this hypothesis. Uncontrolled continuous localized infection including artificial graft infection seems certain to aggravate esophageal wall ischemia and disruption in a similar way.
Eggebrecht et al. reported that they observed mild erosive lesions in the esophagus that led to perforation on endoscopy . This suggested that the lesion took some time to progress to perforation, and ischemic change of the esophageal wall occurred gradually. They also mentioned that recognition of this pre-perforation state could have prompted early triage and/or surgical repair before esophageal perforation.
In no. 5 case, we had recognized redness and erosive change of the esophagus on endoscopy before the aortic replacement. If we had decided esophagectomy at that point, we might avoid poor prognosis of the case.
The prognosis of esophageal perforation cases after aortic replacement/stenting for thoracic aortic dissection or aneurysm is extremely poor especially in the elderly cases. In the elderly cases (over 80 years old), nos. 3, 4, and 5 died 41, 14, and 30 days with sepsis and other severe complications after the esophagectomy, respectively (Table 2.). Therefore, the indication for highly invasive esophagectomy should be decided carefully. We surgeons should restrict the esophagectomy to sustainable patients for invasive surgery in consideration of age and complications. We want to suggest elderly cases over 80 years old should be refrained from the esophagectomy.
It is important to control infection including regional infection and progression of cardiovascular disease for successful treatment as the result of a survival case (no. 1).
Artificial graft/stent with chronic infections was considered to be removed for long survival. We also consider that it is important to perform cardiovascular surgery with attention to maintaining esophageal blood flow.
Vascular-rich tissue filling (muscle flap or omental) to the infection site after esophagectomy may be useful for infection control. Our surviving case underwent intercostal muscle flap filling which could control prosthetic graft infection.