ArticleCureus2024
Black Esophagus: A Life-Threatening Consequence of Hypoperfusion.
Article in Cureus, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- A Case of Black Esophagus in a Patient Presenting With Dyspnea.The Korean journal of helicobacter and upper gastrointestinal research · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute esophageal necrosis (AEN) is an uncommon endoscopic finding characterized by a patchy or diffuse circumferential black pigmentation of the esophageal mucosa, corresponding to ischemic necrosis. It usually presents with upper gastrointestinal bleeding and is thought to be caused by a systemic low blood flow in patients with predisposing risk factors, like advanced age and cardiovascular comorbidities. After initial hemodynamic stabilization, diagnosis is established by esophagogastroduodenoscopy (EGD) with careful biopsies and histological evaluation. Delayed diagnosis is thought to be the main cause of panesophageal necrosis, perforation, mediastinitis and septic shock. We present a case of AEN triggered by hypoperfusion due to severe perioperative blood loss in a 72-year-old woman with a history of cardiovascular disease. Even though she was stabilized during surgery, she still presented with melena 24 hours after, and endoscopic examination showed ischemic patches consistent with AEN. After administering intravenous fluids, proton pump inhibitors (PPI) and parenteral nutrition, a repeat EGD after 72 hours showed a neat improvement with erosive and ulcerative lesions replacing the black patches and a complete healing after eight weeks of oral PPI therapy. AEN is a rare but highly deadly entity that endoscopists must be aware of, especially in patients with multiple comorbidities and presenting with gastrointestinal bleeding after an episode of hemodynamic instability. Quick management can significantly improve survival.
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