Acute esophageal necrosis: A systematic review and pooled analysis

Schizas, Dimitrios; Theochari, Nikoletta A; Mylonas, Konstantinos S.; Kanavidis, Prodromos; Spartalis, Eleftherios; Triantafyllou, Stamatina; Economopoulos, Konstantinos P.; Theodorou, Dimitrios; Liakakos, Theodore

doi:10.4240/wjgs.v12.i3.104

Cited by 23 publications

(36 citation statements)

References 67 publications

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“…The pathogenesis and etiology of AEN are multifactorial that can be related to many factors, such as backflow of gastric contents causing esophageal injury, disruption of the vascular supply leading to hypoperfusion and ischemia, and impaired protective barrier systems due to a weakened immune system and/or a hemodynamically unstable state [ 6 , 7 ]. In a case report study by Khan et al, upper endoscopy revealed AEN (Figure 1 ), starting at the mid esophagus with an abrupt cutoff at the gastroesophageal junction [ 5 ].…”

Section: Reviewmentioning

confidence: 99%

“…The esophagus is structured with an inner mucosal layer lined by a stratified squamous epithelium, submucosa consisting of connective tissue, layers of muscular tissue, and fibrous tissue followed by an outer connective tissue layer [ 6 , 7 ]. The esophagus is unique from other structures in the gastrointestinal system in that it lacks a serosa layer, which is hypothesized to be protective against necrotic damage that can be inflicted [ 6 , 7 ]. The lining of the stomach mucosa is of columnar epithelium and is distinctly separated in the transition from the esophagus with a zig-zag line [ 6 , 7 ].…”

Section: Reviewmentioning

confidence: 99%

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Epidemiology, Pathogenesis, and Clinical Manifestations of Acute Esophageal Necrosis in Adults

Rehman¹,

Jaferi²,

Padda³

et al. 2021

Cureus

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Acute esophageal necrosis (AEN), also termed "black esophagus," is a unique and uncommon occurrence observed in severely sick patients. Other terminologies include acute necrotizing esophagitis and Gurvits syndrome. This condition is described as a darkened distal third of the esophagus observed on endoscopy and presents as an upper gastrointestinal (GI) bleed, difficulty swallowing, abdominal pain, fever, syncope, nausea, and vomiting. The etiology of AEN has been linked to several possibilities, such as excessive gastric acid reflux, hypoperfusion, and ischemia due to impaired vascular supply and hemodynamic instability. Risk factors include increased age, sex (male), heart disease, hemodynamic insufficiency, alcohol use, gastric outlet obstruction, diabetic ketoacidosis (DKA), malnutrition, renal disease, and trauma which also have the propensity to complicate disease course. An esophageal biopsy is not warranted. Treatment of AEN is comprised of supportive management with intravenous fluids, proton pump inhibitors (PPI), sucralfate, parenteral nutrition, and antacids. Management of preexisting comorbidities associated with AEN is crucial to prevent exacerbation of the disease course that could result in a poor prognosis and increased mortality rates. This literature review article comprises epidemiology, etiology, pathogenesis, diagnosis, and management of AEN.

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Section: Reviewmentioning

confidence: 99%

Section: Reviewmentioning

confidence: 99%

Epidemiology, Pathogenesis, and Clinical Manifestations of Acute Esophageal Necrosis in Adults

Rehman¹,

Jaferi²,

Padda³

et al. 2021

Cureus

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“…Surgical intervention is reserved for those who deteriorate despite supportive treatment. 1 Etiology is not yet entirely explained, but diabetic ketoacidosis has been proposed as one among numerous potential triggers. 1 The causative mechanism of injury is hypovolemia and ischemia.…”

Section: Case Reportmentioning

confidence: 99%

“… 1 Etiology is not yet entirely explained, but diabetic ketoacidosis has been proposed as one among numerous potential triggers. 1 The causative mechanism of injury is hypovolemia and ischemia. 1 The most common clinical presentation (85%) is upper gastrointestinal bleeding, which interestingly was not presented in our patient.…”

Section: Case Reportmentioning

confidence: 99%

“… 1 The causative mechanism of injury is hypovolemia and ischemia. 1 The most common clinical presentation (85%) is upper gastrointestinal bleeding, which interestingly was not presented in our patient. 2 We hypothesize that AEN caused microperforations of the esophageal wall which leads to pneumomediastinum and subcutaneous emphysema in our patient.…”

Section: Case Reportmentioning

confidence: 99%

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Acute Esophageal Necrosis as a Cause of Pneumomediastinum in a Patient With Diabetic Ketoacidosis

et al. 2021

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A 36-year-old man with type 1 diabetes was admitted to intensive care unit because of acute respiratory distress. He had a 3 day history of general malaise, vomiting, and diarrhea. On physical examination, the patient was hypotensive (relative risk 100/60 mm Hg), tachycardic (110/min), dyspnoeic (peripheral oxygen saturation of 93%), and signs of subcutaneous emphysema of the neck. Laboratory results demonstrated metabolic acidosis (pH 7.03), hyperglycemia (667.8 mg/dL), acute kidney injury (creatinine 2.7 mg/dL; baseline 0.86 mg/dL), leukocytosis (32.1 3 10 9 ), and increased C-reactive protein (70 mg/L). Hemoglobin was normal (16.5 g/dL). He was intubated shortly after admission. Contrast-enhanced computed tomography (CT) demonstrated an extensive pneumomediastinum with pneumopericardium and subcutaneous emphysema of the anterior thoracic wall and neck (Figure 1). The esophageal wall was diffusely thickened and hypodense. Thoracic CT with ingestion of oral contrast demonstrated no leakage of Figure 1. Contrast-enhanced computed tomography showing an extensive pneumomediastinum with pneumopericardium and subcutaneous emphysema of the anterior thoracic wall and neck.

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