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Acute Esophageal Necrosis (Gurvits Syndrome) Presenting as Globus and Altered Phonation

Patient: Female, 80-year-old Final Diagnosis: Acute esophageal necrosis • acute pharyngitis • duodenal ulcerations • gastric erosions • gastritis Symptoms: Dysphagia • emesis • globus • hoarseness • sore throat Medication:— Clinical Procedure: Esophagogastroduodenoscopy Specialty: Gastroenterology a...

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Detalles Bibliográficos
Autores principales: Deliwala, Smit S., Bala, Areeg, Haykal, Tarek, Elbedawi, Mamoon M., Bachuwa, Ghassan, Gurvits, Grigoriy E.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: International Scientific Literature, Inc. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7491953/
https://www.ncbi.nlm.nih.gov/pubmed/32881843
http://dx.doi.org/10.12659/AJCR.926019
Descripción
Sumario:Patient: Female, 80-year-old Final Diagnosis: Acute esophageal necrosis • acute pharyngitis • duodenal ulcerations • gastric erosions • gastritis Symptoms: Dysphagia • emesis • globus • hoarseness • sore throat Medication:— Clinical Procedure: Esophagogastroduodenoscopy Specialty: Gastroenterology and Hepatology OBJECTIVE: Rare co-existance of disease or pathology BACKGROUND: Acute esophageal necrosis (AEN), also known as black esophagus or Gurvits syndrome, is an infrequently seen clinical condition distinguishable by a visually striking endoscopic appearance of necrotic esophageal mucosa that involves the distal esophagus with proximal extensions ending at the gastroesophageal junction. Since its early recognition pathologically in the 1960s and endoscopically in the 1990s, AEN, despite its rarity, is being increasingly recognized as a demonstratable cause of upper gastrointestinal bleeding. Cases of pan-esophageal necrosis are sparsely reported, leaving management guidance to isolated case reports. CASE REPORT: An 80-year-old female smoker with advanced chronic obstructive pulmonary disease presented with signs and symptoms of acute pharyngitis and globus sensation that had been evolving over the preceding weeks. An esophagogastroduodenoscopy revealed circumferential necrotic mucosa encircling the entire lumen of the esophagus. The patient was made nil-per-os and started on high-dose anti-reflux therapy with adequate hemo-dynamic resuscitation. CONCLUSIONS: AEN is multifactorial but primarily a combination of decreased tissue perfusion and a massive influx of gastric contents in settings of impaired local defense barriers. Despite its dramatic presentation, the majority of cases resolve with conservative medical management, foregoing surgical interventions.