ArticleCureus2026
Acute Esophageal Necrosis Secondary to Cardiogenic Shock: A Case Report and Review of the Literature.
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.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
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), also known as "black esophagus," is an uncommon clinical entity characterized by diffuse, circumferential, dark pigmentation of the esophageal mucosa. Its pathogenesis is explained by a "two-hit" mechanism involving systemic hypoperfusion and local chemical injury from gastric acid. We present the case of a 78-year-old man with a history of hypertension, diabetes, and a recent anteroseptal myocardial infarction complicated by cardiogenic shock, requiring triple stent placement and vasopressor support. One week after discharge, the patient was readmitted due to hematemesis and hemodynamic instability. Upper gastrointestinal endoscopy revealed extensive necrotic tissue in the distal third of the esophagus, ending abruptly at the gastroesophageal junction. A thoracoabdominal computed tomography scan confirmed esophageal wall thickening but ruled out perforation. Management was strictly conservative, consisting of total parenteral nutrition for esophageal rest, aggressive acid suppression with intravenous proton pump inhibitors, and optimization of cardiac output. A follow-up endoscopy performed seven days later showed complete resolution of the necrotic lesions. Although AEN carries a high overall mortality rate, death is usually attributed to underlying comorbidities rather than esophageal complications. This case highlights that prompt stabilization of the triggering hemodynamic event, combined with conservative medical therapy, allows for rapid mucosal recovery and prevents the need for invasive surgical intervention.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.