ArticleCureus2026
Esophageal Exclusion as a Damage-Control Strategy for Acute Esophageal Necrosis Secondary to Ruptured Stanford Type B Aortic Dissection: A Case Report.
Article in Cureus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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3 authors.
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Abstract
Acute esophageal necrosis (AEN) is a rare and life-threatening condition most commonly associated with systemic hypoperfusion and critical illness. Aortic-related AEN is exceptionally uncommon and may result from direct mediastinal compression and vascular compromise rather than generalized hemodynamic insufficiency. We report the case of a 77-year-old man presenting with a Stanford type B aortic dissection associated with aneurysmal degeneration complicated by rupture. The patient presented with progressive dysphagia, back pain, and hemoptysis. Computed tomography angiography demonstrated a large mediastinal hematoma causing marked compression of the thoracic esophagus. Following emergency thoracic endovascular aortic repair (TEVAR), the patient experienced a prolonged intensive care stay complicated by acute respiratory distress syndrome (ARDS) and pulmonary infection. Persistent dysphagia and subsequent gastrointestinal bleeding prompted endoscopic investigation, which revealed progressive esophageal injury evolving from severe erosive esophagitis to transmural necrosis with multiple fistulas and ultimately an aortoesophageal fistula. Given the patient's severe malnutrition, prolonged illness, and mediastinal contamination, esophagectomy was considered prohibitively high risk. Esophageal exclusion and feeding jejunostomy were, therefore, performed as a damage-control strategy to achieve source control. Despite successful diversion of the esophageal stream, the patient died from progressive systemic complications. This case highlights the diagnostic challenge of aortic-related esophageal ischemia and emphasizes that persistent dysphagia, gastrointestinal bleeding, or unexplained inflammatory deterioration following thoracic aortic rupture, dissection, or TEVAR should prompt consideration of esophageal involvement. It also supports the role of esophageal exclusion as a damage-control option in selected high-risk patients who are unsuitable for definitive esophagectomy.
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