Diagnosis and management of acute esophageal necrosis

Abstract

Acute esophageal necrosis is a rare syndrome classically characterized by a striking endoscopic image of diffuse and circumferential black mucosal discoloration of distal esophagus, with an abrupt transition at the gastroesophageal junction and variable proximal extension. The typical patient is an older male with general debilitation and multiple comorbidities presenting with hematemesis or melena. The pathophysiology usually involves a combination of esophageal ischemia, backflow injury from gastric chemical contents and impaired mucosal reparative mechanisms associated with debilitated physical states. It may arise in the setting of hemodynamic compromise, diabetic ketoacidosis, hypothermia, alcoholic intoxication, trauma, inflammatory diseases, esophageal local infection, solid organ transplantation, postoperative status, drugs or acute gastric outlet obstruction, usually in the background of a chronic debilitating process, where the concurrent presence of multiple risk factors, including diabetes mellitus, hypertension, malnutrition, malignancy or alcohol abuse, places a patient at higher risk. The characteristic endoscopic appearance establishes the diagnosis. Biopsy is supportive but not required. Management is mainly supportive and consists of correcting coexisting conditions, fluid therapy, bowel rest, intravenous proton pump inhibitor therapy and red blood cell transfusion as needed. Although this is a serious life-threatening condition, appropriate treatment may result in a favorable outcome in the majority of patients.

Acute esophageal necrosis after kidney transplantation

“…Several drugs have been involved in this pathophysiology of AEN, including non-steroidal anti-inflammatory drugs (NSAID), antihypertensive agents, terlipressin, clozapine, olanzapine, cocaine, and Immunosuppressant agent. [ 1 , 12 ] Esophageal ischemia may be induced by vasoconstrictive agents such as terlipressin, and antihypertensive agents which induce transient low circulatory flow. Immunosuppressant agents like Tacrolimus and MMF compromise gastrointestinal mucosa ability to local defense barrier function and increase the risk of opportunistic infection such as CMV esophagitis.…”

“…Immunosuppressant agents like Tacrolimus and MMF compromise gastrointestinal mucosa ability to local defense barrier function and increase the risk of opportunistic infection such as CMV esophagitis. [ 12 , 13 , 14 ]…”

Acute esophageal necrosis complicated by refractory stricture formation

“…Mucosal injury in AEN results predominantly from a combination of ischemic injury and gastroesophageal acid reflux‐mediated mucosal damage. Most cases occur in patients with underlying cardiovascular comorbidities and alcohol use and are typically associated with cases of severe hemodynamic instability and low‐flow states 3 . Presenting symptoms can include hematemesis, melena, nausea, vomiting, abdominal pain, dysphagia, or odynophagia 4 .…”

Black esophagus: A case of acute esophageal necrosis associated with diabetic ketoacidosis

“…It was first described in the medical literature in 1990 by Goldenberg et al, and was brought into the spotlight in 2007 by Gurvits et al (1,2). In endoscopic examinations, the prevalence of AEN is rare and reported to be up to 0.28% (3,4). The precise etiology of the disease remains unknown, but is presumed to be multifactorial with mucosal ischemia, injury by the reflux of gastric chemical contents, and an impaired mucosal barrier associated with debilitated physical states (3,4).…”

“…In endoscopic examinations, the prevalence of AEN is rare and reported to be up to 0.28% (3,4). The precise etiology of the disease remains unknown, but is presumed to be multifactorial with mucosal ischemia, injury by the reflux of gastric chemical contents, and an impaired mucosal barrier associated with debilitated physical states (3,4). It has been reported that patients usually present multiple comorbidities, the most common being diabetes mellitus, followed by hypertension, alcohol abuse, chronic kidney disease, coronary heart disease, dyslipidemia, peripheral artery disease, malignancy, liver cirrhosis, gastroesophageal reflux disease, congestive heart failure, and chronic obstructive pulmonary disease (5).…”