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Acute Esophageal Necrosis in a Septic Patient with a History of Cardiovascular Disease.

ABSTRACT: Acute esophageal necrosis (AEN), or colloquially named "black esophagus," is a rare clinical condition often associated with ischemic injury to the esophagus secondary to splanchnic vasoconstriction during hypotensive episodes. We present a case of a 78-year-old man with extensive cardiovascular disease who was initially admitted for gallstone pancreatitis and possible cholangitis. His hospital course was complicated by possible sepsis secondary to aspiration pneumonia and hematemesis secondary to acute ischemic esophageal necrosis as noted on upper endoscopy. Interestingly, the patient only had a transient episode of hypotension (approximately 35 minutes) not requiring vasopressor support, which improved with fluid resuscitation, and endoscopic retrograde cholangiopancreatography (ERCP) done 3 days prior showed normal esophageal mucosa. Clinicians should be aware of the possibility of acute esophageal necrosis as a potential etiology of gastrointestinal (GI) bleed in patients with cardiovascular disease and sepsis.

SUBMITTER: Coles M

PROVIDER: S-EPMC7238344 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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Acute Esophageal Necrosis in a Septic Patient with a History of Cardiovascular Disease.

Coles Michael M Madray Victoria V Uy Pearl P

Case reports in gastrointestinal medicine 20200511

Acute esophageal necrosis (AEN), or colloquially named "black esophagus," is a rare clinical condition often associated with ischemic injury to the esophagus secondary to splanchnic vasoconstriction during hypotensive episodes. We present a case of a 78-year-old man with extensive cardiovascular disease who was initially admitted for gallstone pancreatitis and possible cholangitis. His hospital course was complicated by possible sepsis secondary to aspiration pneumonia and hematemesis secondary ...[more]

PMID: 32455033

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Project description:BackgroundShrimp aquaculture has suffered huge economic losses over the past decade due to the outbreak of acute hepatopancreatic necrosis disease (AHPND), which is mainly caused by the bacteria Vibrio parahaemolyticus (V. parahaemolyticus) with the virulence pVA1 plasmid, which encodes a secretory photorhabdus insect-related (Pir) toxin composed of PirA and PirB proteins. The Pir toxin mainly attacks the hepatopancreas, a major metabolic organ in shrimp, thereby causing necrosis and loss of function. The pandemic of antibiotic-resistant strains makes the impact worse.MethodsMild pyrolysis of a mixture of polysaccharide dextran 70 and the crosslinker 1,8-diaminooctane at 180 ℃ for 3 h to form carbonized nanogels (DAO/DEX-CNGs) through controlled cross-linking and carbonization. The multifunctional therapeutic CNGs inherit nanogel-like structures and functional groups from their precursor molecules.ResultsDAO/DEX-CNGs manifest broad-spectrum antibacterial activity against Vibrio parahaemolyticus responsible for AHPND and even multiple drug-resistant strains. The polymer-like structures and functional groups on graphitic-carbon within the CNGs exhibit multiple treatment effects, including disruption of bacterial membranes, elevating bacterial oxidative stress, and neutralization of PirAB toxins. The inhibition of Vibrio in the midgut of infected shrimp, protection of hepatopancreas tissue from Pir toxin, and suppressing overstimulation of the immune system in severe V. parahaemolyticus infection, revealing that CNGs can effectively guard shrimp from Vibrio invasion. Moreover, shrimps fed with DAO/DEX-CNGs were carefully examined, such as the expression of the immune-related genes, hepatopancreas biopsy, and intestinal microbiota. Few adverse effects on shrimps were observed.ConclusionOur work proposes brand-new applications of multifunctional carbon-based nanomaterials as efficient anti-Vibrio agents in the aquatic industry that hold great potential as feed additives to reduce antibiotic overuse in aquaculture.

Project description:The histologic changes associated with acute gastroesophageal reflux disease (GERD) have not been studied prospectively in humans. Recent studies in animals have challenged the traditional notion that reflux esophagitis develops when esophageal surface epithelial cells are exposed to lethal chemical injury from refluxed acid.To evaluate histologic features of esophageal inflammation in acute GERD to study its pathogenesis.Patients from the Dallas Veterans Affairs Medical Center who had reflux esophagitis successfully treated with proton pump inhibitors (PPIs) began 24-hour esophageal pH and impedance monitoring and esophagoscopy (including confocal laser endomicroscopy [CLE]) with biopsies from noneroded areas of distal esophagus at baseline (taking PPIs) and at 1 week and 2 weeks after stopping the PPI medication. Enrollment began May 2013 and follow-up ended July 2015.PPIs stopped for 2 weeks.Twelve patients (men, 11; mean age, 57.6 year [SD, 13.1]) completed the study. Primary outcome was change in esophageal inflammation 2 weeks after stopping the PPI medication, determined by comparing lymphocyte, eosinophil, and neutrophil infiltrates (each scored on a 0-3 scale) in esophageal biopsies. Also evaluated were changes in epithelial basal cell and papillary hyperplasia, surface erosions, intercellular space width, endoscopic grade of esophagitis, esophageal acid exposure, and mucosal impedance (an index of mucosal integrity).At 1 week and 2 weeks after discontinuation of PPIs, biopsies showed significant increases in intraepithelial lymphocytes, which were predominantly T cells (median [range]: 0 (0-2) at baseline vs 1 (1-2) at both 1 week [P?=?.005] and 2 weeks [P?=?.002]); neutrophils and eosinophils were few or absent. Biopsies also showed widening of intercellular spaces (confirmed by CLE), and basal cell and papillary hyperplasia developed without surface erosions. Two weeks after stopping the PPI medication, esophageal acid exposure increased (median: 1.2% at baseline to 17.8% at 2 weeks; ?, 16.2% [95% CI, 4.4%-26.5%], P?=?.005), mucosal impedance decreased (mean: 2671.3 ? at baseline to 1508.4 ? at 2 weeks; ?, 1162.9 ? [95% CI, 629.9-1695.9], P?=?.001), and all patients had evidence of esophagitis.In this preliminary study of 12 patients with severe reflux esophagitis successfully treated with PPI therapy, stopping PPI medication was associated with T lymphocyte-predominant esophageal inflammation and basal cell and papillary hyperplasia without loss of surface cells. If replicated, these findings suggest that the pathogenesis of reflux esophagitis may be cytokine-mediated rather than the result of chemical injury.clinicaltrials.gov Identifier: NCT01733810.

Dataset Information

Acute Esophageal Necrosis in a Septic Patient with a History of Cardiovascular Disease.

Publications

Acute Esophageal Necrosis in a Septic Patient with a History of Cardiovascular Disease.

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